ATP6V1B1 regulates ovarian cancer progression and cisplatin sensitivity through the mTOR/autophagy pathway.

Early detection and effective chemotherapy for ovarian cancer, a serious gynecological malignancy, require further progress. This study aimed to investigate the molecular mechanism of ATPase H+-Transporting V1 Subunit B1 (ATP6V1B1) in ovarian cancer development and chemoresistance. Our data show that ATP6V1B1 is upregulated in ovarian cancer and correlated with decreased progression-free survival. Gain- and loss-of-function experiments demonstrated that ATP6V1B1 promotes the proliferation, migration, and invasion of ovarian cancer cells in vitro, while ATP6V1B1 knockout inhibits tumor growth in vivo. In addition, knocking down ATP6V1B1 increases the sensitivity of ovarian cancer cells to cisplatin. Mechanistic studies showed that ATP6V1B1 regulates the activation of the mTOR/autophagy pathway. Overall, our study confirmed the oncogenic role of ATP6V1B1 in ovarian cancer and revealed that ATP6V1B1 promotes ovarian cancer progression via the mTOR/autophagy axis.

The overexpression of actin related protein 2/3 complex subunit 1B(ARPC1B) promotes the ovarian cancer progression via activation of the Wnt/ß-catenin signaling pathway.

Introduction: Ovarian cancer is one of the most fatal malignancies of the female reproductive system. The purpose of this study is to explore the mechanism of Actin Related Protein 2/3 Complex Subunit 1B(ARPC1B) in the progression of ovarian cancer. Methods: The expressions and prognostic value of ARPC1B in ovarian cancer were identified using the GEPIA database and the Kaplan-Meier Plotter database. The expression of ARPC1B was manipulated to evaluate its impact on the malignant phenotypes of ovarian cancer. The cell proliferation ability was analyzed through CCK-8 assay and clone formation assay. The cell migration and invasion capacity was evaluated through wound healing assay and trans well assay. Mice xenografts were conducted to measure the effects of ARPC1B on tumor development in vivo. Results: Our data suggested that ARPC1B was overexpressed in ovarian cancer, which was correlated with a poorer survival compared to low mRNA expression of ARPC1B in ovarian cancer patients. The overexpression of ARPC1B promoted cell proliferation, migration, and invasion of ovarian cancer cells. Conversely, the knockdown of ARPC1B resulted in the opposite effect. Additionally, ARPC1B expression could activate Wnt/ß-catenin signaling pathway. The administration of the ß-catenin inhibitor XAV-939 abolished the promotion of cell proliferation, migration, and invasion activities induced by ARPC1B overexpression in vitro. Conclusions: ARPC1B was overexpressed in ovarian cancer and was correlated with poor prognosis. ARPC1B promoted ovarian cancer progression through activation of Wnt/ß-catenin Signaling Pathway.

Correlation of vitamin E level during pregnancy with maternal and neonatal health outcomes: a meta-analysis and systematic review.

OBJECTIVE: To investigate maternal vitamin E (tocopherol) levels during pregnancy and maternal and neonatal health (MNH) outcomes by using meta-analysis and systematic review of literature. METHODS: PubMed, Web of Science and Medline database were searched from database establishment to December 2022 to collect studies on the level of vitamin E (tocopherol) and pregnancy outcomes. Seven studies were finally included, after screening based on pre-specified eligibility and exclusion criteria. Included studies must have data on maternal vitamin E levels and maternal and infant pregnancy outcomes. Literature quality assessment was made using the Newcastle-Ottawa-Scale scoring standard, and meta-analysis was performed with the use of RevMan5.3. RESULTS: Seven studies (involving 6247 normal women and 658 adverse pregnancy outcomes women, 6905 total), all with a quality evaluation score ≥6 points, were included. The meta-analysis of the 7 studies revealed the presence of statistical heterogeneity in vitamin E data (P<0.1 and I2>50%), so a random-effects analysis was further carried out. Statistically lower serum vitamin E levels were determined in the adverse pregnancy outcome group compared with the normal group [SMD=4.44, 95% CI (2.44,6.43), P<0.001]. Descriptive analysis of the correlation of vitamin E levels with maternal and neonatal general information showed no statistical difference in vitamin E levels among mothers of different ages (<27 years, ≥27 years), P=0.214; however, women with BMI<18.5 kg/m2 showed a higher incidence of vitamin E deficiency than those with BMI ≥18.5 kg/m2 (χ2=15.173, P<0.05). Maternal vitamin E level with neonatal weight Z-Score >-2 was [1.793 (0.08, 4.514) mg/L], which was significantly lower than that of maternal vitamin E level with neonatal weight Z-Score ≤-2 [2.223 (0.899,6.958) mg/L], P=0.009. Maternal vitamin E levels with neonatal length Z-Score >-2 [1.746 (0.08, 4.514) mg/L] were significantly lower than those with neonatal length Z-Score ≤-2 [2.362 (1.380, 6.958) mg/L], P=0.006. CONCLUSION: Maternal vitamin E level is lower in those with adverse pregnancy outcomes than that in those with non-adverse pregnancy outcomes. Still, given the limited research on the correlation of vitamin E during pregnancy with maternal BMI and neonatal body length and weight, a large-scale and well-designed cohort study is needed for further analysis.