Curcumin-loaded polypropylene/rice husk/SiO2 composites were fabricated with tunable nano-SiO2 filler loadings (0–10 wt%) via melt-blending and injection molding. XRD analysis revealed effective intercalation of nanoparticles and interaction with the polymer chains up to 6 wt% loading. Incorporation of SiO2 fillers significantly enhanced mechanical strength with 6 % nano-SiO2 formulation demonstrating 27 % higher tensile strength, 52 % increased flexural modulus and 51 % greater impact resistance. The silica nanoparticles also reduced heat release rate through protective charring and decreased moisture absorption by over 8 % due to hydrophilic surface groups. In vitro studies showed that curcumin nano-composites with 6 % nano-SiO2 exhibited maximal cytotoxicity against HT-29 and HCT-116 colon cancer cells with CC50 values of 12.4±1.1 μg/ml and 10.3±0.9 μg/ml respectively, attributed to optimal drug release profile. The formulation arrested 22.1% cells in sub-G1 phase inducing apoptosis. Oral administration in tumor-bearing mice led to 3-fold increase in plasma exposure (Cmax 186±14 ng/ml) and relative bioavailability versus free curcumin, indicating capacity to evade presystemic clearance. The composites also enabled 3 times higher tumor accumulation highlighting potential for targeted colorectal cancer therapy via improved pharmacokinetics and site-specific action. Overall, precise tuning of nanostructured fillers augments mechanical and transport properties while potentiating anticancer performance.

This work reports the development of an electrochemical sensor using graphene-peptide conjugates for detecting colorectal cancer (CRC) biomarker leucine-rich alpha-2 glycoprotein-1 (LRG1). To enable LRG1 quantification, we rationally designed peptides with dual graphene anchoring motifs for optimal orientation and binding activity when immobilized on a reduced graphene oxide (rGO) electrochemical transducer surface. The graphene nanomaterial provides several advantages such as high conductivity, large surface area, and excellent stability that can enhance the sensor's analytical performance metrics. Furthermore, the synthetic peptides offer benefits like smaller size, specificity, ease of modification and cost-effective production compared to traditional antibody receptors. Under optimized conditions, the peptide sensor exhibited high sensitivity of 22.3 μA/(ng/mL.cm2), low limit of detection (75 pg/mL LRG1 in serum), accuracy of 101.1 % spiked recovery, and precision within 6 % RSD. Testing with colonoscopy-classified patient serum specimens discriminated normal, precancerous adenomatous polyps and malignant carcinoma stages based on LRG1 overexpression. A 24 % elevation for adenomas and 103 % higher levels in CRC were observed. Validation with spiked plasma samples indicated 97–104 % recovery and <7 % RSD, proving accurate detection capability. Comparison to antibody-based sensors showed superior linear range, sensitivity, reproducibility, and faster assay time. This demonstrates the promise of computational peptide designing combined with advanced nanomaterials for electrochemical detection of CRC progression through serum protein biomarkers.

Background Accumulating evidence has confirmed the role of snoRNAs in a variety of cancer, but rare in renal cell carcinoma (RCC). This study aims to clarify the role of snoRNAs in RCC tumorigenesis and their potential as novel tumor biomarkers. Materials and methods The snoRNA expression matrix was obtained from the public TCGA and SNORic databases. SNORD15A, SNORD35B and SNORD60 were selected and validated by qPCR, then analyzed combined with related clinical factors using T-test and ROC curve. Results All three snoRNAs: SNORD15A, SNORD35B and SNORD60 were significantly upregulated in cancer tissues compared to adjacent tissues from TCGA or FFPE detection. These three snoRNAs were also increased in urinary sediment (US) of RCC as well as the early-stage RCC patients compared with the healthy controls. In addition, RNase stability experiments confirmed their stable existence in US. Meanwhile, the ROC curve shows that SNORD15A, SNORD35B and SNORD60 could effectively distinguish RCC (AUC = 0.7421) and early-stage RCC (AUC = 0.7465) from healthy individuals. Conclusion SNORD15A, SNORD35B and SNORD60 were upregulated in tissues and US of RCC, serving as novel potential biomarkers for RCC diagnosis.

Purpose The credible data about the burden of early-onset colorectal cancer (EOCRC) in China when compared to other countries in the group of twenty (G20) remained unavailable. We aimed to assess the burden and trends of EOCRC and attributable risk factors in China. Meanwhile, the comparison in the burden and attributable risk factors between China and other G20 countries was also evaluated. Methods Data on the incidence, prevalence, mortality, disability-adjusted life years (DALYs), and attributable risk factors of EOCRC in China were obtained from Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 and compared with other G20countries. Temporal trends of age-standardized rates for incidence, prevalence, mortality, and DALYs were evaluated by estimated annual percentage change (EAPC). The autoregressive integrated moving average (ARIMA) model was used to forecast the incidence, mortality, and DALY rates of EOCRC in China from 2020 to 2029. Results From 1990 to 2019, the age-standardized incidence rate (ASIR) and age-standardized prevalence rate (ASPR) of EOCRC in China increased with the EAPCs of 4.61 [95% confidence interval ( CI ): 4.45–4.77] and 5.82 (95% CI : 5.60–6.05). When compared to G20 countries, China was ranked 13 th in the ASIR in 1990 and then increased to 2 nd in 2019, second only to Japan. The ASPRs increased in all G20 countries, being highest in Saudi Arabia, followed by China and Mexico. Moreover, China had the highest age-standardized mortality rate and highest age-standardized DALY rate in 2019. In China, the five leading risk factors, for both sexes, were diet low in milk [18.54% (95% UI: 12.71–24.07)], diet low in calcium [15.06% (95% UI: 10.70–20.03)], alcohol use [12.16% (95% UI: 8.87–15.64)], smoking [9.08% (95% UI: 3.39–14.11)], and diet high in red meat [9.08% (95% UI: 3.39–14.11)] in 2019. Over the next 10 years, ASIR, ASMR, and age-standardized DALY rate of EOCRC will increase continuously in males and females. Conclusion The burden of EOCRC in China and other G20 countries is worrisome, indicating that coordinated efforts are needed to conduct high-quality researches, allocate medical resources, adjust screening guidelines, and develop effective treatment and prevention strategies in the G20 countries.

The ubiquitination process, which involves that binding of an ubiquitin protein to certain substrates, regulates several human biological processes and human cancers. Several studies report that the abnormal expression of quite a few E3 ubiquitin ligases could play critical role in carcinogenic process and cancer progression. In our current study, we identify UHRF1 (Ubiquitin Like with PHD And Ring Finger Domain 1) is an important regulator for breast cancer growth. UHRF1 depletion significantly decreases breast cancer growth in vitro and in vivo. Clinical data analysis reveals that UHRF1 is dramatically elevated in breast cancer, compared to normal breast tissue. UHRF1 correlates with poor survival in luminal type of breast cancer patients, but not in ER-negative groups. The molecular biological studies show that UHRF1 localizes in the nuclear and interact with ERα via its SRA domain, which subsequently inhibits K48-linked ubiquitination of ERα and enhances ERα stability. Our study provides a novel function of UHRF1 in regulation estrogen signaling in breast cancer and a promising target for breast cancer therapeutics.

Background Immune checkpoint inhibitors (ICIs) are dramatically changing the treatment landscape of a variety of cancers. Nevertheless, the variability in ICI responses highlight the importance in identifying predictive biomarkers. PTPRD and PTPRT (PTPRD/PTPRT) are the phosphatases of JAK-STAT signaling, a critical pathway in anti-cancer immunity regulation. However, the pan-cancer association between PTPRD/PTPRT mutation and the efficacy of ICIs remains unclear across pan-cancer patients. Methods We analyzed the association between PTPRD/PTPRT mutations and patient outcomes using clinical data and genomic mutations from TCGA pan-cancer cohort. Furthermore, the ICI-treatment cohort was used to evaluate the relationship between PTPRD/PTPRT mutation and the efficacy of ICIs. Another ICIs-treatment cohort was used to validate the findings. The TCGA pan-cancer dataset was analyzed to explore the correlation between PTPRD/PTPRT mutations and immune signatures. Moreover, we combined four factors to construct a nomogram model that could be used to predict the survival of pan-cancer patients receiving ICI treatment. The calibration curves and area under the curve were applied to assess the performance of the model. Results PTPRD/PTPRT mutations were shown to be associated with a worse prognosis in TCGA cohort ( P < 0.05). In the Samstein cohort, prolonged overall survival (OS) was observed in PTPRD/PTPRT mutant cancers, compared with wild-type cancers (mOS: 40.00 vs 16.00 months, HR = 0.570, 95%CI: 0.479-0.679, P < 0.0001). In the validation cohort, significant OS advantage was observed in PTPRD/PTPRT mutant patients (mOS: 31.32 vs 15.53 months, HR = 0.658, 95%CI: 0.464-0.934, P = 0.0292). Furthermore, PTPRD/PTPRT mutations were associated with a higher tumor mutational burden, MSI score, and TCR score ( P < 0.0001). Enhanced immune signatures were found in the PTPRD/PTPRT mutant cancers ( P < 0.05). Finally, we successfully established a nomogram model that could be used to predict the survival of NSCLC patients who received ICI treatment. Based on the risk score of the model, patients in the low-risk group showed a better mOS than those in the high-risk group (mOS: 2.75 vs 1.08 years, HR = 0.567, 95%CI: 0.492-0.654; P < 0.001). Conclusions PTPRD/PTPRT mutations may be a potential biomarker for predicting ICI treatment responsiveness in multiple cancer types.

BackgroundExosomal miRNA had been proved as the promising biomarkers for multiple cancers including epithelial ovarian cancer (EOC). This study aimed to validate the diagnostic accuracy of exosomal miR-320d, miR-4479, and miR-6763-5p for EOC. Materials and methodsExosomes isolated from the plasma by ultracentrifugation were verified using TEM, qNano and western blot. MiRNAs sequencing was used to screen out the differential exosomal miRNAs and miR-320d, miR-4479, and miR-6763-5p were selected as candidates, which were further verified by RT-qPCR in 168 healthy donors and 161 primary EOC patients. Besides, the diagnostic accuracy of these three exosomal miRNAs were evaluated using the receiver operating characteristic curve (ROC). ResultsMiRNAs sequencing revealed 95 differential exosomal miRNAs between EOC patients and healthy donors. Subsequently, exosomal miR-320d, miR-4479, and miR-6763-5p were significantly down regulated in EOC patients compared with healthy controls and benign patients. More importantly, these three miRNAs could serve as circulating diagnostics biomarkers for EOC, possessing areas under the curve (AUC) of 0.6549, 0.7781, and 0.6834, respectively. Moreover, these three exosomal miRNAs levels were closely associated with lymph node metastasis, meanwhile exosomal miR-320d and miR-4479 expression was related to tumor stage. ConclusionExosomal miR-320d, miR-4479, and miR-6763-5p might serve as potential biomarkers for EOC.

AbstractBackgroundtRNA‐derived fragments (tRFs) have been found to play a regulatory role in the occurrence and development of many tumors. The aim of this study was to identify the expression of tRFs in breast cancer and their ability to serve as diagnostic markers for breast cancer.MethodsTotal RNA was extracted from breast cancer and paracancerous tissues (n = 83), as well as from the sera of breast cancer patients (n = 214) and healthy donors (n = 113) using trizol reagents. Expression of tRFs was then detected by q‐PCR, and analyzed using t‐test and ROC to illuminate their potential as biomarkers for breast cancer.ResultsOur results demonstrated that tRFs: tRF‐Gly‐CCC‐046, tRF‐Tyr‐GTA‐010 and tRF‐Pro‐TGG‐001 were downregulated in both tissues and sera from breast cancer patients as well as early‐stage patients compared with those in the healthy donors. More importantly, the three tRFs were capable of serving as circulating biomarkers of diagnostics and early diagnosis of breast cancer, possessing areas under the curve (AUC) of 0.7871 and 0.7987, respectively.ConclusionstRFs: tRF‐Gly‐CCC‐046, tRF‐Tyr‐GTA‐010 and tRF‐Pro‐TGG‐001 are downregulated in breast cancer and early breast cancer and act as new potential biomarkers for the diagnosis and early diagnosis of breast cancer.

BACKGROUND:Despite the emerging insights into many snoRNAs (small nucleolar RNAs) which are detectable in body fluids and serve as noninvasive biomarkers, few studies have previously discussed the role of snoRNAs in tumor-educated platelets (TEPs). Herein, we systematically estimated dysregulation of snoRNAs in non-small cell lung cancer (NSCLC) and clarified the biomarker potential of SNORD55 in platelets. METHODS:We compared expression of snoRNAs between NSCLC and normal tissues using SNORic datasets. Platelets were isolated from plasma using low-speed centrifugation and subjected to quantitative polymerase chain reaction (qPCR) for SNORD55 detection. RESULTS:SNORD55 was significantly decreased in TEPs from NSCLC patients especially in early-stage patients compared with healthy controls. Importantly, we validated that TEP SNORD55 was capable of acting as a promising biomarker for NSCLC. It exerted diagnostic performance for NSCLC diagnosis, possessing an AUC of 0.803, as well as for early NSCLC diagnosis, possessing an AUC of 0.784. Moreover, the combination of TEP SNORD55 and carcinoembryonic antigen (CEA) improved the diagnostic efficiency of cancer progression. In addition, TEP SNORD55 also potentially acts as a noninvasive early biomarker for lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) with favorable diagnostic efficiencies. CONCLUSIONS:In summary, TEP SNORD55 could potentially serve as a noninvasive biomarker for NSCLC diagnosis and early diagnosis. KEY POINTS:SNORD55 was significantly decreased in TEPs from NSCLC patients compared to healthy controls and acted as a novel biomarker for early NSCLC.

Aim: This study aimed to identify specific and sensitive exosomal miRNAs in diagnosing patients with colorectal cancer (CRC). Methods: Serum exosomes were isolated from 175 CRC patients and 172 healthy donors by ultracentrifugation and identified by transmission electron microscopy, nanoparticle tracking analysis and western blotting. Exosomal miRNA expression was detected by quantitative PCR and the results analyzed by receiver operating characteristic analysis to illuminate the diagnostic accuracy. Results: Both exosomal miR-377-3p and miR-381-3p were downregulated in CRC patients as well as in early-stage patients compared with healthy donors; they could serve as circulating biomarkers of diagnosis, including early diagnosis, for CRC, possessing favorable diagnostic efficiency. Conclusion: Exosomal miR-377-3p and miR-381-3p levels were downregulated in CRC patients and may be useful as novel and specific biomarkers for the diagnosis of CRC, especially early-stage CRC.

BackgroundExosomes derived from cancer cells encapsulate various kinds of tumor-specific molecules and thus can interact with adjacent or distant cells to mediate information exchange. Long non-coding RNAs (lncRNAs) in exosomes have the potential as diagnostic and prognostic biomarkers in different types of cancers. The current study was aimed to identify circulating exosomal lncRNAs for the diagnosis of colorectal cancer (CRC).MethodsExosomes were isolated from the serum by ultracentrifugation and verified by transmission electron microscope (TEM), qNano, and immunoblotting. Exosomal lncRNAs FOXD2-AS1, NRIR, and XLOC_009459 were selected by lncRNA microarray and validated by qPCR in 203 CRC patients and 201 healthy donors. The receiver operating characteristic curve (ROC) was used to assess the diagnostic efficiency of serum exosomal lncRNAs.ResultsExosomal FOXD2-AS1, NRIR, and XLOC_009459 (TCONS_00020073) levels were significantly upregulated in 203 CRC patients and 80 early-stage CRC patients compared to 201 healthy donors, possessing the area under the curve (AUC) of 0.728, 0.660, and 0.682 for CRC, as well as 0.743, 0.660, and 0.689 for early-stage CRC, respectively. Notably, their combination demonstrated the markedly elevated AUC of 0.736 for CRC and 0.758 for early-stage CRC, indicating their potential as diagnostic biomarkers for CRC.ConclusionsOur data suggested that exosomal lncRNAs FOXD2-AS1, NRIR, and XLOC_009459 act as the promising biomarkers for the diagnostics of CRC and early-stage CRC.

Background . Evidence has suggested the functional role of exosomal miRNAs in cancer diagnosis. This study aimed to determine whether the serum exosomal biomarkers can improve the diagnosis of patients with non-small-cell lung cancer (NSCLC). Materials and Methods . The exosomes were extracted from the serum of NSCLC patients ( n  = 235) and healthy donors ( n  = 231) using ultracentrifugation and then were evaluated by using transmission electron microscopy, qNano, and western blotting. The serum exosomal miRNA expression was validated using qPCR. Results . Exosomal miR-620 was significantly reduced in NSCLC and early-stage NSCLC patients ( P < 0.0001) when compared to that of healthy controls, with an area under the curve (AUC) of 0.728 and 0.707, respectively. Exosomal miR-620 expression showed an association with drinking ( P = 0.008) and distant metastasis ( P = 0.037). Additionally, the downregulated exosomal miR-620 showed association with chemotherapeutic effect ( P = 0.044). Conclusion . These findings suggest the serum exosomal miR-620 as a promising diagnostic and prognostic noninvasive biomarker in NSCLC patients.

Circulating exosomal microRNAs (ExmiRNAs) provide an ideal non-invasive method for cancer diagnosis. In this study, we evaluated two circulating ExmiRNAs in NSCLC patients as a diagnostic tool for early-stage non-small lung cancer (NSCLC). The exosomes were characterized by qNano, transmission electron microscopy, and Western blot, and the ExmiRNA expression was measured by microarrays. The differentially expressed miRNAs were verified by RT-qPCR using peripheral blood specimens from NSCLC patients ( n = 276, 0 and I stage: n = 104) and healthy donors ( n = 282). The diagnostic values were measured by receiver operating characteristic (ROC) analysis. The results show that the expression of both ExmiR-20b-5p and ExmiR-3187-5p was drastically reduced in NSCLC patients. The area under the ROC curve (AUC) was determined to be 0.818 and 0.690 for ExmiR-20b-5p and ExmiR-3187-5p, respectively. When these two ExmiRNAs were combined, the AUC increased to 0.848. When the ExmiRNAs were administered with either carcinoembryonic antigen (CEA) or cytokeratin-19-fragment (CYFRA21-1), the AUC was further improved to 0.905 and 0.894, respectively. Additionally, both ExmiR-20b-5p and ExmiR-3187-5p could be used to distinguish early stages NSCLC (0 and I stage) from the healthy controls. The ROC curves showed that the AUCs were 0.810 and 0.673, respectively. Combination of ExmiR-20b-5p and ExmiR-3187-5p enhanced the AUC to 0.838. When CEA and CYFRA21-1 were administered with the ExmiRNAs, the AUCs were improved to 0.930 and 0.928, respectively. In summary, circulating serum exosomal miR-20b-5p and miR-3187-5p could be used as effective, non-invasive biomarkers for the diagnosis of early-stage NSCLC, and the effects were further improved when the ExmiRNAs were combined. Impact statement The high mortality of non-small cell lung cancer (NSCLC) is mainly because the cancer has progressed to a more advanced stage before diagnosis. If NSCLC can be diagnosed at early stages, especially stage 0 or I, the overall survival rate will be largely improved by definitive treatment such as lobectomy. We herein validated two novel circulating serum ExmiRs as diagnostic biomarkers for early-stage NSCLC to fulfill the unmet medical need. Considering the number of specimens in this study, circulating serum exosomal miR-20b-5p and miR-3187-5p are putative NSCLC biomarkers, which need to be further investigated in a larger randomized controlled clinical trial.

Background Small nuclear RNA (snRNA) levels are extremely variable across a wide range of biological conditions. SnRNAs could potentially regulate alternative splicing to drive genetic, dysplastic and neoplastic disease, which might be the main reason for mRNA profile alteration in tumor educated platelets (TEPs). Methods Platelets were isolated from the plasma of lung cancer patients and healthy donors by low-speed centrifugation and subjected to RNA isolation. SnRNA U1, U2, U5 levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Exosomes were isolated by ultracentrifugation and identified by qNano. Results TEP U1, U2, U5 levels were significantly decreased in patients with lung cancer as well as with early stage patients, their downregulation was correlated with lung cancer progression, possessing favorable diagnostic efficiency. More importantly, TEP U1, U2 and U5 levels were closely correlated between paired exosomes and TEP from treated patients but not from untreated ones, and U1, U5 but not U2 in platelets were elevated by apo-exosomes. Conclusion Tumor educated platelet small nuclear RNAs are downregulated and act as promising biomarkers in lung cancer.

To date, microRNA-4709 (miR-4709) has not been studied in colon adenocarcinoma (COAD) on the basis of experiments. In our study, we aimed to investigate the biological roles and clinical significance of miR-4709 in COAD. The expression difference between miR-4709 and NR3C2 was measured based on The Cancer Genome Atlas database and cells. Kaplan-Meier and logrank tests were applied to determine the overall survival (OS) differences according to the miR-4709 and NR3C2 expression levels. To measure whether the miR-4709 level was associated with COAD cell growth, migration, and invasion, we respectively conducted 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, and transwell assays. A luciferase reporter assay was applied to confirm the relationship between miR-4709 and its predicted target. High expression of miR-4709 was found in COAD tissues and cells. The OS rate in the miR-4709 low expression group was significantly higher than that in the miR-4709 high expression group. Univariate and multivariate analyses exhibited that miR-4709 expression was an independent adverse prognostic factor. Exogenous miR-4709 overexpression promoted proliferation, migration, and invasion of LOVO and SW480 cells. Bioinformatics analysis and luciferase assay demonstrated that miR-4709 directly binds to the 3'-untranslated region of NR3C2. NR3C2 was lowly expressed in COAD and high expression of NR3C2 had a better prognosis compared with that in the low expression of NR3C2. Correlation analysis showed that there is a close association between the level of expression of NR3C2 and miR-4709. Accordingly, miR-4709 may function as an oncogene in COAD and provide a preclinical proof for candidate management to target new miR-4709-NR3C2 signaling for COAD therapy.

Background: Let-7d has been reported to serve as a tumor suppressor in numerous cancers, however, the function in rectum adenocarcinoma has not been illuminated. In this study, we aimed to explore whether let-7d functions in rectum adenocarcinoma and its functional significance links to ATP binding cassette subfamily C member 2 (ABCC2). Methods: The expression patterns of let-7d and ABCC2 were gained from TCGA database. Then, cell proliferation, invasion and migration assays were conducted to detect the influence on rectum adenocarcinoma cells behaviors after over-expression of let-7d. Subsequently, the potential target gene of let-7d was predicted and identified through bioinformatics prediction analysis and luciferase reporter assay. Analyses against prognostic value and independent predictor were acquired from Kaplan-Meier, Univariate and Multivariate analysis of Cox regression. Finally, con-transfection experiments were performed to investigate let-7d/ABCC2 pairs function on rectum adenocarcinoma cells after co-transfected with let-7d mimic and si-ABCC2. mRNA and protein levels were assessed by reverse transcription quantitative polymerase chain reaction (qRT-PCR) and western blot. Results: The data from TCGA indicated that let-7d was down-regulated in rectum adenocarcinoma samples, whilst ABCC2 was showed a trend of high expression and its overexpression hinted to worse overall survival of rectum adenocarcinoma patients. Cells proliferation, invasion and migration properties were restrained after over-expression of let-7d in SW837 cells. Further investigations showed that over-expression of let-7d induced the inhibitory effect on SW837 cells proliferative, migrant and invasive capacities was augmented by silencing ABCC2. Conclusions: All results in this study indicated that up-regulation of let-7d could suppress SW837 cells growth, invasion and migration abilities by reducing ABCC2 expression, providing a new insight into molecular mechanism of let-7d/ABCC2 as a significant mediator for tumor progression and development of rectum adenocarcinoma.

The aim of the current study was to investigate and discuss the function of ANKRD33 gene in the pathogenesis of gastric adenocarcinoma. The marked up-regulated expression of ANKRD33 gene in gastric adenocarcinoma tissues compared to normal tissues was found by bioinformatics analysis. Kaplan-Meier analysis revealed that high expression of ANKRD33 is correlated with lower overall survival of gastric adenocarcinoma patients. The results of qPCR revealed that mRNA expression level of ANKRD33 was dramatically higher in AGS, SGC7901, and BGC823 cell lines than that in the GES1 cells. Knockdown of ANKRD33 remarkably inhibited the viability, invasion, and migration of AGS and BGC823 cells. Furthermore, the ratio of p-AKT/AKT and p-mTOR/mTOR was significantly decreased in AGS cells which transfected with si- ANKRD33. All the above results illustrated that ANKRD33 would act as a tumor forwarder in gastric adenocarcinoma development and have a high potential to be a marker molecule in the diagnosis and treatment of gastric tumors.

PURPOSE To screen key modules and explore the potential mechanism of conventional colorectal cancer (CRC) and colorectal serrated adenocarcinoma (SAC). MATERIALS AND METHODS The microarray data of GSE36758 and GSE8671 were downloaded from Gene Expression Omnibus database. The differentially expressed genes (DEGs) in SAC versus colon carcinoma (CC) and CC versus normal control (NC) group were analyzed and the protein-protein interaction (PPI) networks for DEGs were constructed. The modules of PPI networks were further analyzed and the function enrichment analysis of all enrolled DEGs was carried out based on ToppGene database. RESULTS Total eight DEGs (SAC vs. CC) and 445 DEGs (CC vs. NC) were extracted based on the gene expression profile of GSE36758 and GSE8671, respectively. Total three PPI networks were constructed with DEGs in CC versus NC, SAC versus CC group, and DEGs in both two groups. Three modules were extracted from the PPI network of CC versus NC. Meanwhile, three modules were extracted from the network of DEGs in both two groups. Function enrichment analysis showed that DEGs involved in these modules were mainly associated with cellular activities. CONCLUSION DEGs in modules of SAC and CRC were mainly involved in cellular activities pathways. The PPI networks and modules might contribute to the further study of pathogenesis for CRC and SAC based on the molecular level.