OBJECTIVE:To investigate the influence of lactoferrin (LTF) on the anoikis-resistance of nasopharyngeal carcinoma (NPC) cells and explore its relationship with the protein kinase B (AKT) signaling pathway. METHODS:Anoikis-resistant HNE-1 and HONE-1 NPC cell lines were established. The proliferation and survival of cells were detected by Cell Counting Kit-8 (CCK8), while cell cycle and apoptosis were measured by flow cytometry. The transwell assay was used to evaluate invasion and metastasis abilities. The expression of matrix metallopeptidase-9 (MMP-9), vascular endothelial growth factor-A (VEGF-A), E-cadherin and Vimentin were assessed by Western blot. LTF plasmids and LTF shRNA plasmids were transfected into HNE-1 and HONE-1 cells, respectively, and the expression of E-cadherin, Vimentin, AKT and tropomyosin receptor kinase B (TrkB) proteins was detected by Western blot to clarify the role of LTF in anoikis-resistant NPC cells. RESULTS:Anoikis-resistant HNE-1 and HONE-1 NPC cell lines were successfully established. Compared to parental cells, these anoikis-resistant cells exhibited enhanced survival, reduced apoptosis, and significantly increased invasive ability. They also demonstrated elevated expression of VEGF-A, MMP-9, and Vimentin, alongside decreased E-cadherin, indicating epithelial-mesenchymal transition (EMT). Furthermore, the expression of AKT and TrkB was significantly upregulated in anoikis-resistant cells. Critically, LTF overexpression reversed this aggressive phenotype: it suppressed cell survival and invasion, induced G0/G1 cell cycle arrest, promoted apoptosis, and downregulated the expression of AKT and TrkB. Conversely, LTF knockdown produced opposing effects. CONCLUSION:Our study revealed that LTF inhibits anoikis-resistance and metastasis of NPC cells via the AKT signaling pathway.

Natural killer cells (NK) are crucial components of the immune system. NKp30, a significant activation receptor on the NK cell membrane, plays a cytotoxic role by recognizing and binding to corresponding ligands. This interaction mediates the activation of NK cells and the release of regulatory factors, participating in antitumor and anti-infection processes. This review systematically summarizes the structural features and basic functions of NKp30, the impact of N-terminal glycosylation on NKp30 function, related NKp30 ligands and their roles, as well as the antitumor and anti-infective functions and mechanisms of NKp30. The aim is to provide a new perspective for a comprehensive understanding of NKp30 function.

RNA-binding Fox-1 homolog 2 (RBFOX2) is a key RNA-binding protein that primarily functions by regulating alternative splicing. Furthermore, RBFOX2 regulates RNA metabolism across the transcriptional and multiple post-transcriptional stages, encompassing recognizing RNA epigenetic modifications, inhibiting transcription, regulating alternative polyadenylation, inhibiting miRNA processing, and stabilizing mRNA. Additionally, RBFOX2 is regulated by upstream factors such as RNA binding proteins, non-coding RNAs, and transcription factors. RBFOX2 is extensively involved in the regulation of development and the maintenance of physiological functions. The dysregulation of RBFOX2 is closely associated with tumors, cardiovascular diseases, developmental defects and metabolic diseases. In this review, we summarize the regulatory functions of RBFOX2 in terms of both alternative and non-alternative splicing, the upstream regulatory factors of RBFOX2, and its relationship with disease etiology and progression, with the aim of providing a comprehensive understanding of the role of RBFOX2 and offering new insights for the study of RBFOX2.

Insulin-like growth factor 2 messenger RNA (mRNA)-binding protein 2 (IGF2BP2) is a widely studied N6-methyladenosine (m6A) modification reader, primarily functioning to recognize and bind to m6A modification sites on the mRNA of downstream target genes, thereby enhancing their stability. Previous studies have suggested that the IGF2BP2-m6A modification plays an essential role in cellular functions and the progression of various diseases. In this review, we focus on summarizing the molecular mechanisms by which IGF2BP2 enhances the mRNA stability of downstream target genes through m6A modification, thereby regulating cell ferroptosis, epithelial–mesenchymal transition (EMT), stemness, angiogenesis, inflammatory responses, and lipid metabolism, ultimately affecting disease progression. Additionally, we update the related research progress on IGF2BP2. This article aims to elucidate the effects of IGF2BP2 on cell ferroptosis, EMT, stemness, angiogenesis, inflammatory responses, and lipid metabolism, providing a new perspective for a comprehensive understanding of the relationship between IGF2BP2 and cell functions such as ferroptosis and EMT, as well as the potential for targeted IGF2BP2 therapy for tumors and other diseases.

Microtubule-associated protein 1 light chain 3B (MAP1LC3B, also known as LC3B) is a mammalian homolog of the autophagy-related protein 8 (ATG8) family. It plays a crucial role in cellular autophagy and is involved in several vital biological processes, including apoptosis and differentiation. Additionally, LC3B regulates immune responses. Due to its close association with malignant tumors and neurodegenerative diseases, and its potential as a prognostic indicator and therapeutic target, LC3B has become a significant research focus. This article aims to provide a comprehensive and systematic understanding of LC3B's role and mechanisms in autophagy, its impact on apoptosis and the underlying mechanisms, its regulation of cellular differentiation and transdifferentiation, its modulation of immune and inflammatory responses, the influence of upstream regulatory factors on LC3B's function, and its relevance to disease diagnosis, treatment, and prognosis. The goal is to establish a solid foundation for understanding LC3B's role in cellular processes and its regulatory mechanisms.

Pericytes are a type of mural cell located between the endothelial cells of capillaries and the basement membrane, which function to regulate the capillary vasomotor and maintain normal microcirculation of local tissues and organs and have been identified as a significant component in the tumor microenvironment (TME). Pericytes have various interactions with different components of the TME, such as constituting the pre-metastatic niche, promoting the growth of cancer cells and drug resistance through paracrine activity, and inducing M2 macrophage polarization. While changes in the TME can affect the number, phenotype, and molecular markers of pericytes. For example, pericyte detachment from endothelial cells in the TME facilitates tumor cells in situ to invade the circulating blood and is beneficial to local capillary basement membrane enzymatic hydrolysis and endothelial cell proliferation and budding, which contribute to tumor angiogenesis and metastasis. In this review, we discuss the emerging role of pericytes in the TME, and tumor treatment related to pericytes. This review aimed to provide a more comprehensive understanding of the function of pericytes and the relationship between pericytes and tumors and to provide ideas for the treatment and prevention of malignant tumors.

Fos-related antigen 1 (Fra-1) is a nuclear transcription factor that regulates cell growth, differentiation, and apoptosis. It is involved in the proliferation, invasion, apoptosis and epithelial mesenchymal transformation of malignant tumor cells. Fra-1 is highly expressed in gastric cancer (GC), affects the cycle distribution and apoptosis of GC cells, and participates in GC occurrence and development. However, the detailed mechanism of Fra-1 in GC is unclear, such as the identification of Fra-1-interacting proteins and their role in GC pathogenesis. In this study, we identified tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein eta (YWHAH) as a Fra-1-interacting protein in GC cells using co-immunoprecipitation combined with liquid chromatography-tandem mass spectrometry. Experiments showed that YWHAH positively regulated Fra-1 mRNA and protein expression, and affected GC cell proliferation. Whole proteome analysis showed that Fra-1 affected the activity of the high mobility group AT-hook 1 (HMGA1)/phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) signaling pathway in GC cells. Western blotting and flow cytometry confirmed that YWHAH activated HMGA1/PI3K/AKT/mTOR signaling pathway by positively regulating Fra-1 to affect GC cell proliferation. These results will help to discover new molecular targets for the early diagnosis, treatment, and prognosis prediction of GC.

Fos-related antigen-1 (FRA-1) is a member of activator protein-1 (AP-1) transcription factor superfamily, and FRA-1 is highly expressed in colon cancer, breast cancer, gastric cancer, lung cancer, bladder cancer, and other tumors. The expression level of FRA-1 is closely related to the processes of tumor cell proliferation, apoptosis, transformation, migration, and invasion, which is a potential therapeutic target and prognostic factor for many tumors. Clarifying the detailed mechanism of action of FRA-1 could provide the theoretical basis for tumor diagnosis, treatment, and prognosis, and is of great significance for the study of tumor etiology and pathogenesis. In this paper, the expression levels and influencing factors of FRA-1 in various tumor tissues and cells are summarized, as well as the effect of FRA-1 expression level on the biological behavior of tumor cells and the signal transduction mechanism. At the same time, the signal transduction mechanism of FRA-1 in inflammation was expounded. In addition, the related metabolites, drugs and non-coding RNA that affect the expression and function of FRA-1 were summarized. Finally, it illustrates that FRA-1 may be taken as a key factor for tumor prognosis and a potential therapeutic target. This review provides a theoretical basis for the systematic understanding of the relationship between FRA-1 and tumors, its function, and possible mechanism.

Abstract The cell surface receptor CD38 has NADase enzyme and cyclase activity and is necessary for immune cell activation and proliferation. CD38 is a molecular marker for hematological tumor prognosis and diagnosis; however, its role in solid tumors is unclear. This study aimed to explore the role and mechanism of CD38 in the proliferation of solid tumor cells. We found that protein arginine methyltransferase 5 (PRMT5) interacts with CD38 in solid tumor cell lines, resulting in increased levels of CD38. In addition, PRMT5 can methylate CD38 at arginine 58 (R58). Moreover, PRMT5-induced methylation of CD38 affected its enzymatic activity and the NAD level. Finally, in vitro experiments showed that PRMT5-induced methylation of regulates the activity of the CD38-NAD-SIRT1-p53-p21 signal axis to promote the proliferation of solid tumor cells. In summary, PRMT5 promotes malignant tumor cell proliferation by regulating the methylation status of CD38 in solid tumors such as cervical cancer, nasopharyngeal carcinoma, and lung cancer. CD38 R58 could be applied in the early diagnosis and clinical treatment of solid tumors.

In 2019, the national cancer report showed that the incidence rate of gastric cancer (GC) ranked second, only after lung cancer. Its mortality rate ranked third in all tumors. It seriously endangers people' s health. It is very important for reducing the mortality rate of GC to screen and identify early detection markers and search for molecular targets for its treatment. CD90 (THY1) is a cell surface glycoprotein, which plays an important role in tumor cell proliferation, metastasis and angiogenesis. The abnormal expression of CD90 is related to the stem characteristics of cells and promotes the initiation and metastasis of tumor. However, the relationship between CD90 and the stem characteristics of GC cells has not been reported. In this study, we found that CD90 overexpression increased the proportion of side population cells (SP cells) of GC cells AGS. It affected the protein expression levels of stem markers such as ABCG2 and CD105 on the membrane surface, and also affected the mRNA expression levels of stem markers such as NANOG, and SOX2 in GC cells AGS. mRNA microarray and Western blot revealed that CD90 overexpression affected the stem characteristics of GC cells through activating the signal pathway of PI3K/Akt and JNK/ERK1. Our results provide a new idea for the identification of potential molecular targets of gastric cancer.

CD90, also known as Thy-1 cell surface antigen, is located on human chromosome 11q23.3, and encodes a glycosylphosphatidylinositol-linked cell surface glycoprotein. CD90 serves a key role in malignancy by regulating cell proliferation, metastasis and angiogenesis. Gastric cancer is one of the most common types of malignancy. Patients with advanced gastric cancer have a poor prognosis. CD90 plays a key role in the occurrence and progression of gastric cancer. However, the molecular mechanism of CD90 in gastric cancer is currently unclear. In order to identify the molecular mechanism by which CD90 affects the biological behavior and energy metabolism of gastric cancer cells, the present study used Cell Counting Kit-8 assays, lactate concentration determination and ATP content determination. The results demonstrated that CD90 promotes proliferation and inhibits senescence in gastric cancer cells. In addition, CD90 enhanced the invasion and migration abilities of AGS gastric cancer cells. Overexpression of CD90 resulted in the accumulation of intracellular lactic acid in AGS cells. CD90 upregulated lactate dehydrogenase levels and increased the NADPH/NADP+ ratio in AGS cells. CD90 overexpression decreased the ATP concentration in AGS cells. PI3K, PDK1, phosphorylated-AKT-Ser473, HIF-1α, MDM2 and SIRT1 levels were upregulated in CD90-overexpressing AGS cells, compared with AGS cells transfected with the empty vector. In contrast, PTEN, p53, SIRT2, SIRT3 and SIRT6 were downregulated. The results indicate that CD90 affects the biological behavior and levels of energy metabolism of gastric cancer cells by targeting the PI3K/AKT/HIF-1α signaling pathway.

The oncogenesis of cervical cancer is a multi-factor and multi-step process, and major risk factors include oncogene activation with tumor suppressor gene inactivation, viral factors, and immune factors. For example, the human papillomavirus (HPV) has been linked to the occurrence of cervical cancer. At present, the pathogenesis of cervical cancer remains unclear. Fra-1 (Fos-related antigen 1, also known as FOSL1) is a member of the Fos family and an important nuclear transcription factor that regulates normal cell growth, differentiation, and apoptosis. In the present study, we found that Fra-1 inhibited the proliferation of cervical cancer cells while also promoting apoptosis and affecting cell cycle distribution. Moreover, Fra-1 up-regulated STAT1 expression and modulated p53 signal pathway activity in cervical cancer cells. Overexpression of Fra-1 inhibited cell senescence by altering sirtuin 1 (SIRT1) expression in HeLa cells, and Fra-1 overexpression restored mitochondrial disorder and suppressed metabolic reprogramming in HeLa cells. Silencing of STAT1 impaired the inhibitory effect of Fra-1 on cervical cancer cell growth, while knock-down of STAT1 reversed the effect on cell senescence and mitochondrial dysfunction caused by Fra-1 in HeLa cells. Silencing of STAT1 also recovered metabolic reprogramming in cervical cancer cells. In summary, our results show that Fra-1 inhibited cervical cancer cell growth and the Warburg effect via STAT1-mediated regulation of the p53 signaling pathway.

In contrast to normal cells, cancer cells typically undergo metabolic reprogramming. Studies have shown that oncogenes play an important role in this metabolic reprogramming. CD38 is a multifunctional transmembrane protein that is expressed abnormally in a variety of tumor types. To investigate the effect and possible mechanism of CD38 in cervical cancer cells and to provide a new therapeutic target for the treatment of cervical cancer, the present study identified that CD38 is involved in regulating cell metabolism in cervical cancer cells. Liquid chromatography‑tandem mass spectrometry and bioinformatic analyses revealed that differentially abundant proteins in CD38‑overexpressed cervical cancer cells (CaSki‑CD38 and HeLa‑CD38) are predominantly involved in glycolytic pathways, oxidative phosphorylation and the NAD/NADH metabolic process. Further experiments using an ATP test kit and lactate test kit revealed that CD38 promotes glucose consumption, increases lactate accumulation and increases ATP production. In addition, CD38 increases the phosphorylation of phosphatidylserine/threonine kinase (AKT), mechanistic target of rapamycin (mTOR) and phosphatidylinositol‑4,5‑bisphosphate 3‑kinase (PI3K), which play a key role in tumor metabolism. Furthermore, it was found that the energy metabolism of cervical cancer cells was inhibited following treatment with the mTOR inhibitor rapamycin. In conclusion, the results of the present study suggested that CD38 regulates the metabolism of cervical cancer cells by regulating the PI3K/AKT/mTOR pathway, which may be a candidate target for the treatment of cervical cancer.

Objectives This study on all-trans retinoic acid was designed to explore its effect on the ability of Fra-1 to cervical cancer cell development. The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA. Results The results show that the expression of Fra-1 is higher in all-trans retinoic acid-treated cervical cancer. Flow cytometry and kit detection show that all-trans retinoic acid can enhance the ability of Fra-1 to lose the mitochondrial membrane potential, inhibit the glucose consumption and the production of lactic acid as well as ATP. CCK8 and colony formation assays indicate that all-trans retinoic acid enhances the ability of Fra-1 to inhibit cell proliferation. In addition, through Western blot analysis, it was determined that P53 and P21 were up-regulated, and MDM2 and LDHA were down-regulated. Conclusion The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA.

Ovarian cancer is the most common gynecological malignancy that causes cancer-related deaths in women today; this being the case, developing an understanding of ovarian cancer has become one of the major driving forces behind cancer research overall. Moreover, such research over the last 20 years has shown that the Jun N-terminal kinase (JNK) signaling pathway plays an important role in regulating cell death, survival, growth and proliferation in the mitogen-activated protein kinases (MAPK) signaling pathway, an important pathway in the formation of cancer. Furthermore, the JNK signaling pathway is often regulated by an abnormal activation in human tumors and is frequently reported in the literature for its effect on the progression of ovarian cancer. Although the FDA has approved some JNK inhibitors for melanoma, the agency has not approved JNK inhibitors for ovarian cancer. However, there are some experimental data on inhibitors and activators of the JNK signaling pathway in ovarian cancer, but related clinical trials need to be further improved. Although the Jun N-terminal kinase (JNK) signaling pathway is implicated in the formation of cancer in general, research has also indicated that it has a role in suppressing cancer as well. Here, we summarize this seemingly contradictory role of the JNK signaling pathway in ovarian cancer, that ‘seesaws’ between promoting and suppressing cancer, as well as summarizing the application of several JNK pathway inhibitors in cancer in general, and ovarian cancer in particular.

To better understand the role of integrin subunit alpha 9 (ITGA9) gene polymorphism in epithelial ovarian cancer (EOC), we investigated the distribution of ITGA9 gene polymorphisms (rs2212020 and rs189897) and revealed whether these polymorphisms were associated with a curative effect in EOC. It was found that rs2212020 and rs189897 were correlated significantly with EOC incidence. The frequency of the C allele of rs2212020 was significantly higher in EOC patients than in the control group (P = 0.009, χ2 = 6.857). The population with the C allele of rs2212020 had a higher EOC risk than the population with the T allele (hazard ratio = 1.97, 95.0% CI = 1.178-3.299). Further, our results showed that the CC genotype was a risk factor for EOC. Regarding the association between ITGA9 and the sensitivity to platinum-based chemotherapy in EOC, there were no statistically significant differences in the frequencies of the rs189897 and rs2212020 polymorphisms between the chemosensitive group and the control group. In multivariate analysis, the patients with the TT genotype of rs189897 had longer progression free survival (PFS) than the patients without this genotype (P = 0.010, OR = 2.491). The AT genotype of rs189897 was a risk factor for PFS in EOC. These findings suggested that rs189897 and rs2212020 could play important roles in EOC diagnosis and prognosis.

The incidence and mortality rates of hepatocellular carcinoma (HCC) are higher in China compared with in other countries. Further research is required in order to improve the diagnosis and treatment of HCC. Sperm-associated antigen 9 (SPAG9) protein has been revealed to serve an important function in cancer progression; however, the underlying mechanisms remain to be elucidated. The present study investigated the expression level of SPAG9 in HCC tissues using quantitative-polymerase chain reaction, immunohistochemistry and western blotting, and the results demonstrated that SPAG9 was overexpressed in HCC tissues compared with the adjacent non-cancerous tissues. To explore the potential mechanisms underlying SPAG9 in HCC, the effect of SPAG9 on cell proliferation, cell cycle, migration and invasion capacities were investigated in the QGY HCC cell line by RNA interference. It was revealed that inhibition of SPAG9 mRNA in QGY cells significantly inhibited the expression level of SPAG9 compared with the control. Depletion of SPAG9 expression decreased cell proliferation (P<0.01) and increased the percentage of cells in the G(1)/G(2) cell cycle phase. The percentage of cells in the S phase was decreased, and cell migration and invasion capabilities in vitro were reduced (P<0.01). In summary, the results of the present study suggested that SPAG9 was upregulated in HCC and may serve an important function in cancer cell proliferation, differentiation and invasion. Whether SPAG9 is a potential diagnostic marker and therapeutic target of human HCC requires additional study.

Cervical cancer is one of the most common malignant tumors in women all over the world. The exact mechanism of occurrence and development of cervical cancer has not been fully elucidated. CD38 is a type II transmembrane glycoprotein, which was found to mediate diverse activities, including signal transduction, cell adhesion, and cyclic ADP‐ribose synthesis. Here, we reported that CD38 promoted cell proliferation and inhibited cell apoptosis in cervical cancer cells by affecting the mitochondria functions. We established stable cervical cancer cell lines with CD38 over‐expressed. CCK8 assay and colony formation assay indicated that CD38 promoted cervical cancer cell proliferation. Nude mouse tumorigenicity assay showed that CD38 significantly promotes tumor growth in vivo. CD38 also induced S phase accumulation in cell cycle analysis and suppressed cell apoptosis in cervical cancer cells. Meanwhile, flow cytometry analysis of mitochondria functions suggested that CD38 decreased intracellular Ca2+ levels in cervical cancer cells and CD38 was involved in down‐regulation of ROS levels and prevented mitochondrial apoptosis in cervical cancer cells. The percentage of cells with loss of mitochondrial membrane potential (Δψm) in CD38‐overexpressed cervical cancer cells was less than control groups. Furthermore, we found an up‐regulation of MDM2, cyclinA1, CDK4, cyclinD1, NF‐kB P65, c‐rel, and a downregulation of P53, P21, and P38 by Western blot analysis. These results indicated that CD38 enhanced the proliferation and inhibited the apoptosis of cervical cancer cells by affecting the mitochondria functions.

Cervical cancer is one of the most common malignant tumors in women all over the world. However, the exact etiology of cervical cancer remains unclear. The receptor for activated protein kinase C (RACK1) is reported to be involved in tumorigenesis and tumor progression. Besides, the prognostic value of RACK1 in several kinds of tumors has been identified. However, there are limited studies on the functional role of RACK1 in cervical cancer. In this study, we tested the expression level of RACK1 by immunohistochemistry and western blot technologies and find that it is upregulated in cervical cancer. Colony formation and CCK8 assays indicate that RACK1 promotes cell proliferation in CaSki cervical cancer cells. While the silence of RACK1 decreases the cell proliferation in CCK8 analysis. beta-galactosidase staining suggests that RACK1 decreases cell senescence in cervical cancer cells. Invasion and migration assay show that RACK1 promotes the invasion and migration of cervical cancer cells. Also, when RACK1 was silenced, it exerts the opposite result. Furthermore, the mRNA expression levels of MMP-3, MMP-9 and MMP-10 were upregulated in RACK1-overexpressed CaSki cells by qPCR analysis. RACK1 also induces S phase accumulation in cell cycle analysis and suppresses cell apoptosis in cervical cancer cells. Flow cytometry analysis of mitochondria functions suggests that RACK1 increases the mitochondrial membrane potential (Delta psi m) levels to prevent mitochondrial apoptosis in cervical cancer cells. To explore the possible mechanism of RACK1, we tested and found that RACK1 upregulates the expression of NF-kappa B, cyclin D1 and CDK4 and downregulates the expression of p53, p38, p21 and STAT1 in cervical cancer cells. These results suggest that RACK1 promotes cell growth and invasion and inhibits the senescence and apoptosis in cervical cancer cells probably by affecting the p53 pathway.

Cancer testis antigen sperm-associated antigen 9 (SPAG9) is highly expressed in many types of cancers. In the present study, to obtain a better understanding of the relevance of SPAG9 in cancer diagnosis and treatment, the expression of SPAG9 mRNA and protein in lung cancer specimens was evaluated by RT-PCR, western blotting and immunohistochemistry. ELISA was used to quantify the SPAG9 autoantibody in the peripheral blood of lung cancer patients. The results showed that the expression of SPAG9 mRNA and protein in the lung cancer tissues was significantly higher than that in the adjacent non-cancerous tissues (P<0.01). The level of the SPAG9 autoantibody in the serum of lung cancer patients was significantly higher than the level in the healthy controls (P<0.001), and the level of the SPAG9 autoantibody in the serum of untreated patients was significantly higher than that in treated patients (P=0.002). SPAG9 IgG antibody levels were significantly lower in treated adenocarcinoma and small cell lung cancer patients than these levels in the untreated patients (P=0.006, P=0.026, respectively), while no statistical difference was found between treated and untreated squamous cell carcinoma patients. Our results suggest that the SPAG9 antibody in serum is a promising marker for the diagnosis of lung cancer, and the level of the humoral immune response to this antigen appears to be related to the type of lung cancer.