Adipose-derived stem cells are widely used in aging field because of their extensive sources, low immunogenicity and strong secretory function. In particular, the exosomes of adipose-derived stem cells are rich in small molecules of RNA and protein. Studies have shown that exosomes also play a role in regulation of ER stress. Therefore, we hypothesized that exosomes of adipose-derived stem cells could regulate ER stress and delay fibroblasts senescence. In this study, we use H2O2 to promote cellular senescence and treat with adipose-derived stem cell exosomes. The function of cell proliferation and apoptosis were compared, and the levels of validating factor and collagen were detected. Then we explored the mechanism of action of exosomes derived from adipose-derived stem cells. We found adipose-derived stem cell exosomes could inhibit fibroblast senescence, including promoting cell proliferation, inhibiting apoptosis and regulating collagen secretion, by regulating ER stress through SIRT1. To further validate the relevance of this mechanism at the population level, public human skin transcriptomic data were analyzed, revealing coordinated downregulation of SIRT1 expression and unfolded protein response (UPR) signaling during physiological skin aging, with a strong positive correlation between SIRT1 expression and UPR pathway activity. This study suggests that adipose-derived stem cell exosomes attenuate stress-induced senescence-like changes in fibroblasts, highlighting their potential relevance in the modulation of cellular aging.

This multicentre, two-arm, phase 2 study aimed to explore the efficacy and safety of neoadjuvant camrelizumab plus chemotherapy or apatinib in patients with initially unresectable stage II-III non-small-cell lung cancer (NSCLC). Eligible patients regardless of PD-L1 expression received neoadjuvant camrelizumab 200 mg and platinum-doublet chemotherapy every 3 weeks (arm A) or those with PD-L1-positive tumors received neoadjuvant camrelizumab and apatinib 250 mg once daily (arm B), for 2-4 cycles, followed by surgery. The primary endpoint was major pathological response (MPR) rate. Thirty patients in arm A and 21 in arm B were enrolled. Surgery rates were 50.0% (15/30) in arm A and 42.9% (9/21) in arm B, with all patients achieving R0 resections. Of these patients, the MPR and pathological complete response rates were both 20.0% (95% CI 4.3-48.1) in arm A and were 55.6% (95% CI 21.2-86.3) and 11.1% (95% CI 0.3-48.2) in arm B, respectively. The corresponding objective response rates were 33.3% (95% CI 11.8-61.6) and 55.6% (95% CI 21.2-86.3). With a median follow-up of 22.4 months (95% CI 19.0-26.0), the median event-free survival was not reached (NR; 95% CI 13.6-NR) in arm A and 16.8 months (95% CI 8.6-NR) in arm B. Grade 3 or above treatment-related adverse events occurred in eight (26.7%) patients in arm A and three (14.3%) in arm B. Biomarker analysis showed baseline TYROBP expression was predictive of treatment response in arm B. Neoadjuvant camrelizumab plus chemotherapy or apatinib exhibits preliminary efficacy and manageable toxicity in patients with initially unresectable stage II-III NSCLC.

Lung squamous cell carcinoma (LUSC) is the second most common type of non-small cell lung cancer. Toosendanin can target critical cancer cell survival and proliferation. However, the function of toosendanin in LUSC is limited. Cancer cell proliferative capacity is detected using cell morphology, colony formation, and flow cytometry. The invasiveness of the cells is detected by a Transwell assay, western blotting, and RT-qPCR. Nude mice are injected with H226 (1×10 6 ) and received an intraperitoneal injection of toosendanin every 2 days for 21 days. RNA sequence transcriptome analysis is performed on toosendanin-treated cells to identify target genes and signaling pathways. With increasing concentrations of toosendanin, the rate of cell proliferation decreases and apoptotic cells increases. The number of migrated cells significantly reduces and epithelial-mesenchymal transition is reversed. Injection of toosendanin in nude mice leads to a reduction in tumor volume, weight, and the number of metastatic tumors. Furthermore, KEGG shows that genes related to the AMPK pathway are highly enriched. BNIP3 is the most differentially expressed gene, and its expression along with phosphorylated-AMPK significantly increases in toosendanin-treated cells. Toosendanin exerts anticancer effects, induces apoptosis in LUSC cells, and inhibits tumor progression via the BNIP3/AMPK signaling pathway.

Pancreatic cancer is a malignancy with a poor prognosis and high mortality. The lincRNA TMPOP2 is highly expressed in gynecological cancers and may exhibit tumor-promoting functions. However, the function of TMPOP2 in pancreatic cancer is limited. TMPOP2 expression in pancreatic cancer and adjacent tissues is analyzed from The Cancer Genome Atlas (TCGA) and GTEx database. It shows the high expression of TMPOP2 in pancreatic cancer tissues. Similar results are observed in resected pancreatic adenocarcinoma tumors and adjacent tissues from 20 patients and the relative cell lines. When the pancreatic cell lines are transfected with si-TMPOP2, it shows that TMPOP2 downregulation inhibits the cells migration and EMT. Furthermore, the potential mechanism is explored by detecting the expression of c-Jun N-terminal kinase (JNK), phosphorylated JNK, signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3. It suggests that TMPOP2 knockdown inactivates JNK and STAT3 phosphorylation. When a JNK activator (anisomycin) is added to the cells with si-NC or si-TMPOP2, it can partially reverse the migration and EMT inhibition of the cells with inhibited TMPOP2. TMPOP2 inhibition suppresses the migration and EMT of pancreatic cancer by repressing the JNK/STAT3 pathway. Thus, this may be a novel target for pancreatic cancer therapy.

Background: The role of ferroptosis in breast cancer brain metastasis (BCBM) is unclear. This study aimed to explore the ferroptosis-related genes (FRG) relations with the tumor microenvironment, as well as evaluate their values in predicting survival and drug sensitivity in patients with BCBM.Materials and Methods: Genes expression and clinical data were downloaded from Gene Expression Omnibus (GEO). Univariate and multivariate Cox regression analyses were performed to explore the independent prognostic factors. Consensus cluster principal component analysis (PCA) was used to establish the ferroptosis score. Immunological signatures were analyzed by the single-sample gene set enrichment analysis (ssGSEA). Drug sensitivity was evaluated through the estimated half-maximal inhibitory concentration (IC50). Finally, results were validated in external cohorts.Results: Fourteen significantly different FRG were identified between breast cancer (BC) and BCBM tissues. Survival analysis demonstrated HMOX1, PEBP1, KEAP1, and LPCAT3 were significantly associated with overall survival (OS) and relapse-free survival (RFS) (all p < 0.05). High ferroptosis score was correlated with iron ion homeostasis, iron metabolism, higher stromal cells and immune cells scores. Patients with high- and low-ferroptosis scores were characterized by different drug sensitivities. Following external validations, the ferroptosis had distinct expression profiles between the BC and BCBM, and could serve as biomarkers for OS and drug response.Conclusion: Our findings suggested that ferroptosis may be involved in the process of BCBM, and ferroptosis could serve as prognostic biomarkers. Evaluation of ferroptosis may deepen our understanding about the tumor microenvironment, and could help clinicians to make individualized therapy.

BackgroundLung adenocarcinoma is one of the common causes of cancer-related deaths worldwide. Histone cluster 1 H2A family member b (HIST1H2AB) is a member of the histone H2A family. Bioinformatic analyses have revealed that HIST1H2AB is highly expressed in some cancers and might be an oncogene. However, information on the function of HIST1H2AB in lung adenocarcinoma is limited. MethodsThe expression of HIST1H2AB was analyzed in normal lung, lung adenocarcinoma and paracancerous tissues from The Cancer Genome Atlas (TCGA) database and immunohistochemistry staining. It was further verified in the relative cell lines using real-time quantitative polymerase chain reaction (RT-qPCR). When the adenocarcinoma cells lines (A549 and H1299) were successfully transfected with shHIST1H2AB or an empty plasmid packaged into a lentivirus, cell proliferation was detected using Celigo fluorescence cell-counting, colony formation and annexin V-allophycocyanin assays. Twenty nude mice were subcutaneously injected with A549 cells transfected with shHIST1H2AB or empty plasmid; the tumor size was recorded on day 25 and then measured every 3 days thereafter. The final tumor weight was measured on day 37. Significantly differentially expressed genes were analyzed using a human gene expression array. Furthermore, the potentially relevant genes were verified using RT-qPCR and western blotting. ResultsHIST1H2AB was highly expressed in lung adenocarcinoma tissues from TCGA database and immunohistochemistry staining. Similar results were seen in the lung adenocarcinoma cells. When the cells were successfully transfected with shHIST1H2AB or an empty plasmid, downregulation of HIST1H2AB inhibited the growth and promoted the apoptosis of lung adenocarcinoma cells. The xenograft results suggested that HIST1H2AB downregulation delayed tumor growth and reduced tumor weight. Moreover, interferon signaling pathway and four genes (HMGB1, FOXM1, F2RL1 and SLC4A7) might be regulated by HIST1H2AB in the development of lung adenocarcinoma as indicated through gene expression array, RT-qPCR and western blotting analyses. ConclusionsHIST1H2AB acts as an oncogenic protein and HIST1H2AB inhibition suppresses the proliferation of lung adenocarcinoma cells. It may be a novel target for lung adenocarcinoma therapy.

医疗质量同质化是"一院多区"医院管理工作中的难点.同济大学附属东方医院通过搭建"一院两区"医疗质量管理信息平台,充分借助信息化手段,实现医疗质量管理委员会、医疗质量管理部门、临床科室三级联动的闭环管理模式,助力提升院区间医疗质量同质化水平.

Background Lung squamous cell carcinoma (LUSC) is prone to metastasis and likely to develop resistance to chemotherapeutic drugs. DNA repair has been reported to be involved in the progression and chemoresistance of LUSC. However, the relationship between LUSC patient prognosis and DNA damage repair genes is still unclear. Methods The clinical information of LUSC patients and tumour gene expression level data were downloaded from the TCGA database. Unsupervised clustering and Cox regression were performed to obtain molecular subtypes and prognosis-related significant genes based on a list including 150 DNA damage repair genes downloaded from the GSEA database. The coefficients determined by the multivariate Cox regression analysis and the expression level of prognosis-related DNA damage repair genes were employed to calculate the risk score, which divided LUSC patients into two groups: the high-risk group and the low-risk group. Immune viability, overall survival, and anticarcinogen sensitivity analyses of the two groups of LUSC patients were performed by Kaplan-Meier analysis with the log rank test, ssGSEA and the pRRophetic package in R software. A time-dependent ROC curve was applied to compare the survival prediction ability of the risk score, which was used to construct a survival prediction model by multivariate Cox regression. The prediction model was used to build a nomogram, the discriminative ability of which was confirmed by C-index assessment, and its calibration was validated by calibration curve analysis. Differentially expressed DNA damage repair genes in LUSC patient tissues were retrieved by the Wilcoxon test and validated by qRT-PCR and IHC. Result LUSC patients were separated into two clusters based on molecular subtypes, of which Cluster 2 was associated with worse overall survival. A prognostic prediction model for LUSC patients was constructed and validated, and a risk score calculated based on the expression levels of ten DNA damage repair genes was employed. The clinical utility was evaluated by drug sensitivity and immune filtration analyses. Thirteen-one genes were upregulated in LUSC patient samples, and we selected the top four genes that were validated by RT-PCR and IHC. Conclusion We established a novel prognostic model based on DNA damage repair gene expression that can be used to predict therapeutic efficacy in LUSC patients.

Background: Many biological clocks related to aging have been linked to the development of cancer. A recent study has identified that the inflammatory aging clock was an excellent indicator to track multiple diseases. However, the role of the inflammatory aging clock in glioblastoma (GBM) remains to be explored. This study aimed to investigate the expression patterns and the prognostic values of inflammatory aging (iAge) in GBM, and its relations with stem cells. Methods: Inflammation-related genes (IRG) and their relations with chronological age in normal samples from the Cancer Genome Atlas (TCGA) were identified by the Spearman correlation analysis. Then, we calculated the iAge and computed their correlations with chronological age in 168 patients with GBM. Next, iAge was applied to classify the patients into high- and low-iAge subtypes. Next, the survival analysis was performed. In addition, the correlations between iAge and stem cell indexes were evaluated. Finally, the results were validated in an external cohort. Results: Thirty-eight IRG were significantly associated with chronological age (|coefficient| > 0.5), and were used to calculate the iAge. Correlation analysis showed that iAge was positively correlated with chronological age. Enrichment analysis demonstrated that iAge was highly associated with immune cells and inflammatory activities. Survival analysis showed the patients in the low-iAge subtype had significantly better overall survival (OS) than those in the high-iAge subtype (p < 0.001). In addition, iAge outperformed the chronological age in revealing the correlations with stem cell stemness. External validation demonstrated that iAge was an excellent method to classify cancer subtypes and predict survival in patients with GBM. Conclusions: Inflammatory aging clock may be involved in the GBM via potential influences on immune-related activities. iAge could be used as biomarkers for predicting the OS and monitoring the stem cell.

-BACKGROUND: CXC motif chemokine receptor type 4 (CXCR4) is an indispensable factor in the process of lung cancer brain metastasis (LCBM). The PI3K/AKT signal pathway is crucial in affecting cell invasion and metas-tasis and serves as a pivotal regulator in LCBM. However, the relationship between CXCR4 and the PI3K/AKT signal pathway is unclear. This study aimed to explore the un-derlying mechanisms of CXCR4 and PI3K/AKT in LCBM. -METHODS: Two lung cancer cells (A549 and H1299) and cells transfected with short hairpin RNA (shRNA)-CXCR4 were cocultured with normal human astrocyte cells and human brain endothelial (hCMEC/D3) cells to establish a blood-brain barrier model in vitro. The proliferation, migration, and invasion tight junction proteins (claudin-5, occludin, and ZO-1) were examined. Finally, results were verified in a nude mice model.-RESULTS: The abilities of cell proliferation, migration, and invasion were significantly reduced in A549 and H1299 cells transfected with shRNA-CXCR4 compared with the negative control group. The proteins phosphorylated PI3K and phosphorylated AKT were downregulated in lung cancer cells transfected with shRNA-CXCR4. The proteins claudin-5, occludin, and ZO-1 were upregulated in the A549 and H1299 cells transfected with shRNA-CXCR4. In vivo experiment results confirmed that the knockdown of CXCR4 played a protective role in the process of LCBM.-CONCLUSIONS: Our findings revealed that CXCR4 pro-motes LCBM by regulating the PI3K/Akt signal pathway. We also demonstrated that inhibiting CXCR4 could lead to prevention of LCBM. This study provides further rationale for clinical therapy that targets CXCR4/PI3K/AKT.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic and advanced interstitial lung disease with poor prognosis. AHNAK nucleoprotein 2 (AHNAK2) is a macromolecular protein that is important for cell migration and muscle membrane repair. The protein acts via epithelial-mesenchymal transition (EMT), which is a key mechanism in the pathogenesis of IPF. However, very few studies have elucidated the effect of AHNAK2 in the development of IPF. Therefore, we aimed to determine the role of AHNAK2 in IPF development. Methods: C57BL/6 mice were induced with bleomycin, while A549 and Beas-2b pulmonary epithelial cell lines were treated with TGF-beta 1 to induce IPF model. The expression of AHNAK2 was detected using immunohistochemistry staining in vivo, and real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting (WB) in vitro. C57BL/6 mice were injected with adeno-associated virus (AAV)-sh NC or AAV-sh AHNAK2 and the pulmonary function and EMT marker expression were measured. The migratory abilities of the two transforming growth factor beta 1 (TGF-beta 1)-induced cell lines were examined using wound-healing and Transwell assays after transfection with si-NC, si-AHNAK2-1 and -2. EMT marker expression was detected using RT-qPCR and WB. Smad3 and phosphorylated-Smad3 of the two cells were examined using WB. Following Smad3 inhibition by Smad3 phosphorylation inhibitor (SIS3), TGF-beta 1-induced cell migration and EMT marker expression were evaluated again after different transfections. Results: AHNAK2 expression was higher in the IPF model than in the normal model in vivo and in vitro. Partial inhibition of AHNAK2 suppressed the EMT process and improved pulmonary ventilation and compliance in the mouse model of IPF. Similarly, knockdown of AHNAK2 suppressed the migration of pulmonary epithelial cells and reversed EMT. Furthermore, Smad3 of the two TGF-beta 1-induced cell lines was not activated when AHNAK2 was inhibited. When SIS3 inhibited the activation of Smad3, the suppression of AHNAK2 had no effect on A549 and Beas-2b, regardless of TGF-beta 1 induction. Conclusions: Inhibition of AHNAK2 alleviates pulmonary fibrosis and partially reverses EMT by inhibiting the TGF-beta 1/Smad3 signaling pathway. Therefore, AHNAK2 is a potential therapeutic target for IPF.

Abstract Objective The aim of this study was to assess the efficacy and safety of intrapleural perfusion with hyperthermic chemotherapy (IPHC) in treating malignant pleural effusion (MPE) compared to normothermic chemoperfusion of the pleural cavity (NCPC), and to investigate the better treatment to control MPE. Methods Malignant pleural effusion patients were enrolled in the study and treated with NCPC or IPHC under video‐assisted thoracoscopic surgery (VATS). The chest drainage duration, clinical characteristics, and recurrence time of pleural effusion of patients were collected for statistical analysis. The chi‐squared test and the Fisher's exact test were applied to compare the distribution differences in categorical variables. Progression‐free survival (PFS) was estimated by the Kaplan–Meier method and was compared by the log‐rank test. The survival analysis was performed using the Cox proportional hazards method. Results A total of 37 MPE patients were enrolled in this study. Twenty‐seven patients received NCPC and 10 patients received IPHC under VATS. Significant differences were found in pathological types (p = 0.011), chest drainage duration (p = 0.005), and remission rate (p = 0.009) between two different treatment groups. The chest drainage duration of IPHC under VATS was shorter than the NCPC group (t = 2.969, p = 0.005). The remission rate of MPE in IPHC group was better than the NCPC one (OR = 0.031, 95% CI: 0.002–0.507, p = 0.015). The result of the Kaplan–Meier method showed that IPHC group could significantly prolong the PFS of patients with MPE compared to NCPC group (log‐rank p = 0.002). Univariate cox regression analysis showed that patients with MPE in the IPHC group presented significant longer PFS than the NCPC group (HR = 0.264, 95% CI: 0.098–0.713, p = 0.009). Multivariate cox regression analysis further verified this conclusion (HR = 0.268, 95% CI: 0.096–0.753, p = 0.012). Conclusion Compared to the NCPC, the IPHC under VATS presents a better control effect on MPE, shorter tube placement time, and longer complete remission time. For this reason, we recommend IPHC under VATS as the first‐line treatment for patients with MPE those who can tolerate minimally invasive surgery.

Background: This study was to evaluate the value of lobectomy in the prognosis of Non-small cell lung cancer (NSCLC) patients with primary metastasis based on the Surveillance Epidemiology and End Results (SEER) database. Methods: This was a population-based retrospective study and the clinical data were collected from the National Cancer Institute's SEER database between 2010 and 2015. The effects of pulmonary surgery and surgical procedures on lung cancer-specific survival (LCSS) and overall survival (OS) were assessed, and the COX regression models were employed to evaluate the survival of primary surgery in patients with primary metastatic NSCLC (pmNSCLC) and the survival of surgical procedure in pmNSCLC patients. Results: A total of 55,717 patients diagnosed with pmNSCLC between 2010 and 2015 were enrolled, and pulmonary surgery was indicated in 1,575 (2.83%) patients. Surgery was an independent risk factor for LCSS (P < 0.001, HR 0.658, 95%CI: 0.637–0.680) and OS (P < 0.001, HR 0.665, 95%CI: 0.644–0.686) of pmNSCLC patients. The surgery was associated with better OS (P < 0.001, HR 0.678, 95%CI: 0.657–0.699). The site of metastasis was also related to the survival after primary tumor surgery (P = 0.001). As compared to the sublobectomy and pneumonectomy, lobectomy improved the LCSS for NSCLC patients with single-organ metastasis, rather than multiple metastases (P < 0.001). In patients receiving sublobectomy, lobectomy, and pneumonectomy, the median LCSS was 12, 28, and 13 months, respectively, and the 5-year LCSS rate was 14.39, 32.06, and 17.24%, respectively. Conclusion: The effect of locoregional surgery on the survival of pmNSCLC patients with single-organ metastasis has been underestimated, and lobectomy may be a preferred treatment for patients with single-lung metastasis.

目的 探讨食管癌和贲门癌术后复发或再发胸食管-胃癌(thoracic esophageal-gastric cancer,TEGC)的临床特点及胸内消化道二次重建术的安全性和有效性.方法 回顾性分析2007年7月至2019年12月接受内镜复查的353例食管癌和贲门癌术后患者的临床资料.共发现31例(8.78％)术后复发或再发TEGC患者,其中男24例、女7例,平均年龄58.5(42～68)岁;其中腺癌18例(58.06％)、鳞状细胞癌13例(41.94％),且均接受了TEGC切除及胸内消化道二次重建术.随访胸腹部CT与上消化道造影检查,对于可疑患者进行胃镜检查;随访时间截至患者死亡或2019年12月30日.采用Kaplan-Meier方法计算生存率,生存分析采用log-rank检验.结果 本组31例患者在接受了TEGC切除之后,再行胸内消化道二次重建术,其中残胃-食管胸内吻合术8例、结肠代食管术13例、空肠代食管术6例(其中食管-空肠Roux-en-Y吻合1例)、颈部食管-胃吻合术4例.患者平均手术时间为404.8(340～475)min;术中平均出血量为378.4(180～620)mL;术后并发症4例,其中肺部感染3例、颈部切口感染1例;术后平均住院时间为17.1(14～21)d.所有入组患者均获得随访,11例Ⅰ～ⅡA期患者中位生存时间为25(19.8～35.0)个月,20例ⅡB～ⅢA期患者中位生存时间为16(12.5～19.5)个月,两者差异有统计学意义(x2=7.840 8,P＜0.01).结论 食管癌和贲门癌术后存在复发或再发TEGC,多为异时胃癌或残留食管床肿瘤复发侵及胸胃壁所致,术后定期内镜复查是主要方法.对TEGC患者再手术进行胸内消化道二次重建术的治疗在技术上安全可行,可使患者生存获益.

运用FOCUS-PDCA分析我院POCT血糖仪管理工作的始末环节,查找POCT血糖仪质量管理系统化建设的关键影响因素.通过完善和落实POCT血糖仪的管理制度,改进和优化血糖仪管理流程,建立POCT血糖仪质量管理信息平台,并将POCT血糖仪质量管理上升至全院质量管理的重点环节,最终在患者安全、工作效率、经济社会效益均取得良好成效.

Additional file 8: Table S8. KEGG analysis of up-regulated RBPs.

Additional file 7: Table S7. GO analysis of up-regulated RBPs.

Background: It has been demonstrated by studies globally that autophagy took part in the development of cervical cancer (CC). Few studies concentrated on the correlation between overall survival and CC patients. We retrieved significant autophagy-related genes (ARGs) correlated to the process of cervical cancer. They may be used as prognosis marker or treatment target for clinical application. Methods: Expressions level of genes in cervical cancer and normal tissue samples were obtained from GTEx and TCGA database. Autophagy-related genes (ARGs) were retrieved accroding to the gene list from HaDB. Differentially expressed autophagy related genes (DE-ARGs) related to cervical cancer were identified by Wilcoxon signed-rank test. ClusterProfiler package worked in R software was used to perform GO and KEGG enrichment analyses. Univariate propotional hazard cox regression and multivariate propotional hazard cox regressions were applied to identify DE-ARGs equipped with prognostic value and other clinical independent risk factors. ROC curve was drawn for comparing the survival predict feasibility of risk score with other risk factors in CC patients. Nomogram was drawn to exhibit the prediction model constructed accroding to multivariate cox regression. Correlations between Differentially expressed autophagy related genes (DE-ARGs) and other clinical features were investigated by t test or Cruskal wallis analysis. Correlation between Immune and autophagy in cervical cancer was investigated by ssGSEA and TIMER database. Results: Fifty-six differentially expressed ARGs (DE-ARGs) were retrieved from cervical cancer tissue and normal tissue samples. GO enrichment analysis showed that these ARGs involved in autophagy, ubiquitination of protein and apoptosis. Cox regression medel showed that there were six ARGs significantly associated with overall survival of cervical caner patients. VAMP7 (HR = 0.599, P= 0.033) and TP73 (HR = 0.671, P= 0.014) played protective roles in survival among these six genes. Stage (Stage IV vs Stage I HR = 3.985, P<0.001) and risk score (HR = 1.353, P< 0.001) were sorted as independent prognostic risk factors based on multivariate cox regression. ROC curve validated that risk score was preferable to predict survival of CC patients than other risk factors. Additionally, we found some of these six predictor ARGs were correlated significantly in statistic with tumor grade or stage, clinical T stage, clinical N stage, pathology or risk score (all P< 0.05). The immune cells and immune functions showed a lower activity in high risk group than low risk group which is distincted by median risk score. Conclusion: Our discovery showed that autophagy genes involved in the progress of cervical cancer. Many autophagy-related genes could probably serve as prognostic biomarkers and accelerate the discovery of treatment targets for CC patients.

Esophageal squamous cell carcinoma (ESCC) is the most common and aggressive tumor worldwide, and the long-term survival of these patients remains poor. Three databases (GSE17351, GSE20347, and GSE100942) were obtained from Gene Expression Omnibus, and 193 differentially expressed genes including 56 upregulated and 137 downregulated genes were identified by paired test using limma R package. Then, functional enrichments by gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses showed these genes were mainly related protein digestion and absorption, and IL-17 signaling pathway. We then constructed a protein-protein interaction network and cytoHubba module to determine the six hub genes and overall survival analysis of the six hub genes were evaluated by UALCAN and GEPIA2 analysis. Ultimately, the experimental results confirmed the KIF4A was overexpressed in the ESCC tissues and cell lines compared with the normal esophageal mucosal tissues and was linked to poor prognosis. Moreover, we also revealed that KIF4A facilitates proliferation, cell cycle, migration, and invasion of ESCC in vivo and in vitro. Overall, these findings demonstrated that KIF4A could serve as diagnostic and prognostic biomarkers and may help facilitate therapeutic targets in ESCC patients.