Yuhong Wang

Telomerase reverse transcriptase gene polymorphisms and cervical cancer susceptibility in high‐risk human papillomavirus‐infected women

AbstractObjectiveTo investigate the relationship between Human telomerase reverse transcriptase (hTERT) gene polymorphisms and the susceptibility and clinicopathological parameters of cervical cancer in women infected with high‐risk human papillomavirus (HR‐HPV).MethodA total of 380 patients with HPV‐infected cervical cancer who were admitted to the Jilin province Maternal and Child Health Care Hospital (Jilin province Obstetrics Quality Control Center) from July 2019 to July 2023 were selected as case group, and 408 women with negative HPV results in the cervical cancer screening results of the physical examination in the same hospital were selected as the control group. Restriction fragment length polymorphisms polymerase chain reaction was used to detect the polymorphisms of hTERT, and its relationship with the susceptibility to high‐risk HPV infection and clinicopathological parameters in patients with cervical cancer was analysed.ResultsIndividuals carrying the GA and AA genotypes of rs2736122 were significantly associated with an increased risk of cervical cancer when compared with the GG genotype and the adjusted ORs were 0.53 (0.37–0.79) for the AA genotype and 0.73 (0.59–0.88) for the A allele genotype. Besides, GG genotype or G allele of rs2853677 presented a significant influence on cervical cancer, with ORs of 0.59 (0.41–0.86) and 10.77 (0.63–0.94), respectively, when compared with the AA genotype. And rs2853677 have statistically significant difference in tumour diameter and degree of differentiation subgroup(p < 0.05).ConclusionThe results of this study indicate that the hTERT gene rs2736122AA and rs2853677 GG genotypes can increase the susceptibility of high‐risk HPV infection in cervical cancer patients. And rs2853677 is related to tumours above 4 cm and highly differentiated tumours. But both have nothing to do with the patient's chemotherapy sensitivity.

PABPC3 drives ovarian cancer metastasis and drug sensitivity by downregulating CLDN1 expression

Abstract Ovarian cancer remains one of the most lethal malignancies affecting women, with its high mortality rate primarily attributed to the aggressive metastatic nature of the disease, leading to late-stage diagnoses. The challenges posed by tumor metastasis and treatment resistance significantly complicate disease management and substantially reduce survival rates. Thus, elucidating the mechanisms underlying ovarian cancer metastasis is crucial for developing targeted therapies and improving patient outcomes. In this study, through single-nucleus RNA sequencing and analysis of clinical samples, we identify PABPC3 as a key regulator of ovarian cancer metastasis and patient survival. Functional experiments reveal that PABPC3 knockdown markedly inhibits ovarian cancer cell proliferation and migration, whereas its overexpression exerts the opposite effects. Furthermore, in vivo models confirm that PABPC3 overexpression significantly enhances metastatic potential. Mechanistically, PABPC3 promotes tumor metastasis by modulating the expression of CLDN1, a critical component of tight junctions. PABPC3 knockdown leads to a significant upregulation of CLDN1, while simultaneous CLDN1 knockdown partially rescues the migration-inhibitory effects induced by PABPC3 depletion. Additionally, clinical analyses demonstrate that high PABPC3 expression correlates with shorter overall survival, even among patients receiving chemotherapy. Notably, increased PABPC3 protein levels in metastatic lesions are associated with reduced progression-free survival. In conclusion, this study underscores the pivotal role of PABPC3 in ovarian cancer metastasis and patient prognosis, highlighting it as a potential therapeutic target for improving clinical outcomes.