To investigate the effects of transmembrane protein 45A (TMEM45A) on biological characteristics and cisplatin (DDP) resistance of cervical cancer cells. TMEM45A in cervical cancer cells and normal cervical epithelial cells (HCerEpiC) were quantified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. HPV genotypes were identified by multiplex PCR. SiHa and HeLa cells were divided into Blank, shCTL, shTMEM45A-1, and shTMEM45A-2 groups, followed by Cell Counting Kit-8 (CCK-8), EdU, Annexin V-FITC/PI staining, Wound healing, and Transwell invasion assays, as well as qRT-PCR and Western blotting. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide) was employed to evaluate the impact of TMEM45A shRNA on cisplatin-resistant cervical cancer cells (SiHa/DDP and HeLa/DDP). Compared with HcerEpic cell, cervical cancer cells exhibited the upregulation of TMEM45A expression, especially in HPV-positive cell lines (CaSki, SiHa, HeLa). TMEM45A shRNA suppressed the proliferation of SiHa and HeLa cells, arrested cells at the S phase, and promoted cell apoptosis. TMEM45A shRNA inhibited the epithelial-mesenchymal transition (EMT), invasion, migration of SiHa and HeLa cells, accompanying by the downregulated Vimentin and N-cadherin with the upregulated E-cadherin. Moreover, SiHa/DDP and HeLa/DDP had higher TMEM45A expression than their parental SiHa and HeLa cells, respectively. And inhibiting TMEM45A can reduce the IC50 of SiHa/DDP cells and HeLa/DDP cells to cisplatin. Silencing TMEM45A can inhibit cell proliferation, invasion, migration and EMT, regulate cell cycle distribution, promote cell apoptosis, and reverse cisplatin resistance of HPV-positive cervical cancer cells, highlighting that inhibition of TMEM45A may be a therapeutic strategy for HPV-positive cervical cancer.

探讨跨膜蛋白45A（TMEM45A）对宫颈癌细胞生物学特性及顺铂（DDP）耐药性的影响。通过定量实时聚合酶链反应 (qRT-PCR) 和蛋白质印迹法对宫颈癌细胞和正常宫颈上皮细胞 (HCerEpiC) 中的 TMEM45A 进行定量。HPV基因型通过多重PCR鉴定。SiHa和HeLa细胞分为Blank、shCTL、shTMEM45A-1、shTMEM45A-2组，依次为Cell Counting Kit-8 (CCK-8)、EdU、Annexin V-FITC/PI染色、伤口愈合、Transwell侵袭化验，以及 qRT-PCR 和蛋白质印迹。MTT (3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide) 用于评估 TMEM45A shRNA 对顺铂耐药宫颈癌细胞 (SiHa/DDP 和 HeLa/DDP) 的影响。与 HcerEpic 细胞相比，宫颈癌细胞表现出 TMEM45A 表达上调，特别是在 HPV 阳性细胞系（CaSki、SiHa、HeLa）中。TMEM45A shRNA抑制SiHa和HeLa细胞的增殖，使细胞停滞在S期，促进细胞凋亡。TMEM45A shRNA 抑制上皮间质转化 (EMT)、SiHa 和 HeLa 细胞的侵袭、迁移，伴随着下调的波形蛋白和 N-钙粘蛋白与上调的 E-钙粘蛋白。此外，SiHa/DDP 和 HeLa/DDP 的 TMEM45A 表达量分别高于其亲本 SiHa 和 HeLa 细胞。而抑制TMEM45A可以降低SiHa/DDP细胞和HeLa/DDP细胞对顺铂的IC50。沉默TMEM45A可以抑制细胞增殖、侵袭、迁移和EMT，调节细胞周期分布，促进细胞凋亡，