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Ovarian cancer is one of the most common malignant tumours affecting the female reproductive organs. CD147 (BSG) and CD98hc (SLC3A2) are oncogenes that form the CD98hc-CD147 complex, which regulates the proliferation, metastasis, metabolism, and cell cycle of cancer cells. The roles of the CD98hc-CD147 complex in ovarian cancer remain unclear. We analysed the expression and prognostic value of CD147 and CD98hc in ovarian cancer using the TCGA and ICGC databases. The effect of CD147 and CD98hc on the tumour immune response was analysed using the TIMER database. CD98hc was more highly expressed in normal tissues than primary tumour tissues, while CD147 was more highly expressed in primary tumour tissues than normal tissues. CD98hc expression was significantly associated with neutrophil and dendritic cell levels. CD147 and CD98hc were correlated with DNA repair, the cell cycle, and DNA replication. The CD98hc-CD147 complex could serve as a target for ovarian cancer treatment.

Background/Aims: Extensive studies have demonstrated that Bleomycin (BLM) is a glycopeptide antibiotic that has been used as an anticancer chemotherapeutic reagent. It can induce both single- and double-strand DNA damage, inhibit synthesis of DNA, suppress proliferation, and induce apoptosis in cancer cells. Smad signaling transducers are considered as important molecules in tumor development and progression, and may closely be related to the biological behaviors of some malignant carcinomas, including gastric cancer. Methods: The effects of different concentrations of BLM on the proliferation, cell cycle, apoptosis, migration, and invasion on gastric cancer cell lines MKN45 and AGS were assayed by using CCK-8 assay, Annexin V/PI double staining, PI staining, and transwell assay. Western blot and Immunohistochemistry were applied to analyze the potential mechanism(s). Results: BLM treatment resulted in a low proliferation, high apoptosis, low migration and invasion in MKN45 and AGS cells. Furthermore, the possible mechanisms underlying that Smad3 activity could be changed after binding with BLM, and subsequently the Smad signaling pathway had a cascade response. Conclusion: These results highlight BLM as an exciting theme for gastric cancer treatment, which may represent an effective clinical therapeutic reagent for gastric cancer patients.

Background: Gastric cancer is one of the most common cancers in the world. MAC30/Transmembrane protein 97 (TMEM97) is aberrantly up-regulated in many human carcinoma cells. However, the function of MAC30 in gastric carcinoma cells is not studied. Material and Methods: To investigate the function of MAC30 in gastric carcinoma, we used RNA silencing technology to knock down the expression of MAC30 in gastric cancer cells BGC-823 and AGS. Real-time quantitative PCR and Western blot were used to analyze the mRNA level and the related protein expression. The localization of MAC30 and lamellipodia was observed by immunofluorescence. The biological phenotypes of gastric cells were examined by cell proliferation assay, cell cycle analysis, apoptosis assay, cell migration and invasion assay. Results: We found that down-regulation of MAC30 expression efficiently inhibited the proliferation of gastric cancer cells. Furthermore, the mobility of gastric cancer cells was also inhibited by down-regulation of MAC30. Moreover, we found that MAC30 knockdown inhibited AKT phosphorylation and reduced the expression of cyclinB1 and WAVE2. Conclusion: To our knowledge, this is the first report investigating the effect of MAC30 on growth, cell cycle, migration, and invasion in gastric carcinoma cells via suppressing AKT signaling pathway. MAC30 may be a potential therapeutic target for treatment of gastric carcinoma.

COL4A3 protein belongs to type IV collagen family and is closely linked to kidney diseases and cancer. To clarify the roles of COL4A3 in gastric carcinogenesis and subsequent progression, its expression was examined by immunohistochemistry on tissue microarrays containing gastric carcinomas, adjacent intestinal metaplasia, pure intestinal metaplasia, and gastritis. Gastric carcinoma tissue and cell lines were studied for COL4A3 expression by Western blotting and reverse transcription--polymerase chain reaction. We found that COL4A3 was differentially expressed in GES-1, AGS, BGC-823, GT-3 TKB, HGC-27, KATO-III, MGC-803, MKN28, MKN45, SCH, SGC-7901, and STKM-2 at both messenger RNA and protein levels. Carcinomas showed statistically lower COL4A3 expression than matched nonneoplastic mucosa (P < .05). Expression was strong in intestinal metaplasia in comparison with gastritis and carcinoma (P < .05). There was greater COL4A3 expression in carcinoma than gastritis (P < .05). Expression of COL4A3 protein was positively correlated with tumor size, lymphatic invasion, venous invasion, and TNM stage (P < .05). There was more COL4A3 expression in diffuse than in intestinal-type carcinomas regardless of invasion into the muscularis propria (P < .05). Histologically, all signet ring cell (n = 43) and mucinous (n = 12) carcinomas showed COL4A3 expression. Kaplan-Meier analysis indicated that COL4A3 expression was negatively associated with a favorable prognosis of overall, advanced, and intestinal-type gastric carcinomas (P < .05). Aberrant COL4A3 expression might play an important role in the pathogenesis and subsequent progression of gastric carcinoma. COL4A3 overexpression might be used as a marker of gastric intestinal metaplasia and mucinous and signet ring cell carcinoma. [ABSTRACT FROM AUTHOR]