Erratum to: circRNA circSnx12 confers Cisplatin chemoresistance to ovarian cancer by inhibiting ferroptosis through a miR-194-5p/SLC7A11 axis.

[Erratum to: BMB Reports 2023; 56(3): 184-189, PMID: 36617466, PMCID: PMC10068343] The BMB Reports would like to correct in BMB Rep. 56(3): 184-189, titled "circRNA circSnx12 confers Cisplatin chemoresistance to ovarian cancer by inhibiting ferroptosis through a miR-194-5p/SLC7A11 axis". The original version of this article unfortunately contained image error in the Fig. 3. This article has been updated to correct an error in the image in Fig. 3D. The author apologizes for any inconvenience or confusion this error may cause. Author information has been modified in the original PDF version.

Expression of mitochondrial transcription factor A in granulosa cells: implications for oocyte maturation and in vitro fertilization outcomes.

OBJECTIVE: In vitro fertilization-embryo transfer (IVF-ET) is a widely used treatment for infertility, with oocyte maturation and quality having a significant impact on oocyte fertilization, embryo development, and fetal growth. Mitochondrial transcription factor A (TFAM) is essential for maintaining the mitochondrial oxidative respiratory chain and supplying energy for oocyte development, fertilization, and embryonic development. In this study, we aimed to examine TFAM expression in women undergoing IVF-ET and assess its impact on the IVF outcomes. METHODS: We recruited 85 women who underwent IVF-ET treatment for infertility. On the date of egg collection, granulosa cells were extracted from the clear follicular fluid of the first mature egg using ultrasound-guided needle aspiration. The collected granulosa cells served three purposes: (1) detecting TFAM gene expression in granulosa cells via immunocytochemistry, (2) determining TFAM mRNA expression using reverse transcription-PCR (RT-PCR), and (3) measuring TFAM protein expression through western blotting. RESULT: Based on the results, we found that TFAM was localized and expressed in the cytoplasm of granulosa cells, whereas no expression was detected in the nucleus. Granulosa cells exhibited a linear correlation between TFAM mRNA and TFAM protein expression. The study participants were divided into three groups using the ternary method based on relative TFAM mRNA expression thresholds of 33% and 76%: the low-expression group (n = 30), the moderate-expression group (n = 27), and the high-expression group (n = 28). When compared to the other two groups, the moderate expression group exhibited a significantly higher egg utilization rate, 2 pronucleus rate, fertilization rate, and clinical pregnancy rate (P < 0.05). CONCLUSION: TFAM was detected in the cytoplasm of human ovarian granulosa cells. Women with moderate TFAM expression demonstrate enhanced outcomes in IVF.

A retrospective analysis of the effect of latent tuberculosis infection on clinical pregnancy outcomes of in vitro fertilization-fresh embryo transferred in infertile women.

In areas with high incidence of tuberculosis (TB), there are more infertile women who underwent in vitro fertilization (IVF) and have latent TB infection (LTBI), and thus, their potential risks should be paid enough attention. The purpose of our study aimed to analyze the relationship between LTBI and clinical pregnancy outcomes of IVF and fresh embryo transfer (IVF-FET). This was a retrospective study of 628 infertile women who had undergone IVF-FET in the Fourth Affiliated Hospital of Hebei Medical University from January 2019 to December 2021. The women experienced no clinical symptoms, negative imaging, and T-SPOT.TB-positive diagnosis of LTBI. We divided the study population into the LTBI group and the non-LTBI group. The clinical pregnancy rate in the LTBI group was significantly lower than that in the non-LTBI group (40.54% vs 49.51%, P = 0.031), and there was no significant difference in live birth rate and miscarriage rate between the two groups. Logistic regression analysis showed that LTBI was an independent risk factor for decreased clinical pregnancy rate in infertile women undergoing IVF-FET. In conclusion, LTBI affects clinical pregnancy rate of IVF-FET in infertile women, and therefore, clinicians (especially in countries with a high TB burden) need to pay attention to LTBI before IVF and embryo transfer.

Expression of circ-PHC3 enhances ovarian cancer progression via regulation of the miR-497-5p/SOX9 pathway.

BACKGROUND: Accumulating studies have reported indispensable functions of circular RNAs (circRNA) in tumor progression through regulation of gene expression. However, circRNA expression profiles and functions in human ovarian carcinoma (OC) are yet to be fully established. METHODS: In this research, deep sequencing of circRNAs from OC samples and paired adjacent normal tissues was performed to establish expression profiles and circ-PHC3 levels between the groups further compared using RT-qPCR. The effects of ectopic overexpression of miR-497-5p and SOX9 and siRNA-mediated knockdown of circ-PHC3 and an miR-497-5p inhibitor were explored to clarify the regulatory mechanisms underlying circ-PHC3 activity in OC proliferation and metastasis. Information from public databases and the luciferase reporter assay were further utilized to examine the potential correlations among circ-PHC3, miR-497-5p and SOX9. RESULTS: Our results showed significant upregulation of circ-PHC3 in both OC cell lines and tissues. In the luciferase reporter assay, downregulation of circ-PHC3 led to suppression of metastasis and proliferation, potentially through targeted effects on the miR-497-5p/SOX9 axis in OC. SOX9 overexpression or miR-497-5p suppression rescued OC cell proliferation and invasion following silencing of circ-PHC3. Moreover, SOX9 inhibition induced restoration of OC cell invasion and proliferation under conditions of overexpression of miR-497-5p. Thus, circ-PHC3 appears to exert effects on cancer stem cell differentiation through regulation of the miR-497-5p/SOX9 axis. CONCLUSION: Taken together, our findings suggest that circ-PHC3 enhances OC progression through functioning as an miR-497-5p sponge to promote SOX9 expression, supporting its potential as a promising candidate target for OC therapy.

Erratum to: circRNA circSnx12 confers Cisplatin chemoresistance to ovarian cancer by inhibiting ferroptosis through a miR-194-5p/SLC7A11 axis.

[Erratum to: BMB Reports 2023; 56(3): 184-189, PMID: 36617466, PMCID: PMC10068343] The BMB Reports would like to correct in BMB Rep. 56(3): 184-189, titled "circRNA circSnx12 confers Cisplatin chemoresistance to ovarian cancer by inhibiting ferroptosis through a miR-194-5p/SLC7A11 axis". This research has the wrong affiliation of the authors and number of affiliation. Since author's affiliation is incorrect, this information has now been corrected as follows. Kaiyun Qin1,3,#, Fenghua Zhang2,#, Hongxia Wang1, Na Wang1, Hongbing Qiu4, Xinzhuan Jia1,5, Shan Gong1 & Zhengmao Zhang1,* 1Department of Gynecology, Fourth Hospital of Hebei Medical University, Hebei Shijiazhuang 050011, 2Department of Breast & Thyroid Surgery, Hebei General Hospital, Hebei Shijiazhuang 050057, 3Department of Gynecology, Hebei General Hospital, Hebei Shijiazhuang 050057, 4Department of Gynecology, Hebei Xingtai People's Hospital, Hebei Shijiazhuang 054001, 5Department of Reproductive Medicine, Fourth Hospital of Hebei Medical University, Hebei Shijiazhuang 050011, China The author apologizes for any inconvenience or confusion this error may cause. Author information has been modified in the original PDF version.

miR-141-3p accelerates ovarian cancer progression and promotes M2-like macrophage polarization by targeting the Keap1-Nrf2 pathway.

The miR-141-3p has been reported to participate in regulating autophagy and tumor-stroma interactions in ovarian cancer (OC). We aim to investigate whether miR-141-3p accelerates the progression of OC and its effect on macrophage 2 polarization by targeting the Kelch-like ECH-associated protein1-Nuclear factor E2-related factor2 (Keap1-Nrf2) pathway. SKOV3 and A2780 cells were transfected with miR-141-3p inhibitor and negative control to confirm the regulation of miR-141-3p on OC development. Moreover, the growth of tumors in xenograft nude mice treated by cells transfected with miR-141-3p inhibitor was established to further testify the role of miR-141-3p in OC. The expression of miR-141-3p was higher in OC tissue compared with non-cancerous tissue. Downregulation of miR-141-3p inhibited the proliferation, migration, and invasion of ovarian cells. Furthermore, miR-141-3p inhibition also suppressed M2-like macrophage polarization and in vivo OC progression. Inhibition of miR-141-3p significantly enhanced the expression of Keap1, the target gene of miR-141-3p, and thus downregulated Nrf2, while activation of Nrf2 reversed the reduction in M2 polarization by miR-141-3p inhibitor. Collectively, miR-141-3p contributes to tumor progression, migration, and M2 polarization of OC by activating the Keap1-Nrf2 pathway. Inhibition of miR-141-3p attenuates the malignant biological behavior of ovarian cells by inactivating the Keap1-Nrf2 pathway.

circRNA circSnx12 confers Cisplatin chemoresistance to ovarian cancer by inhibiting ferroptosis through a miR-194-5p/SLC7A11 axis.

Ovarian cancer (OC) is the most common gynecological malignancy worldwide, and chemoresistance occurs in most patients, resulting in treatment failure. A better understanding of the molecular processes underlying drug resistance is crucial for development of efficient therapies to improve OC patient outcomes. Circular RNAs (circRNAs) and ferroptosis play crucial roles in tumorigenesis and resistance to chemotherapy. However, little is known about the role(s) of circRNAs in regulating ferroptosis in OC. To gain insights into cisplatin resistance in OC, we studied the ferroptosis-associated circRNA circSnx12. We evaluated circSnx12 expression in OC cell lines and tissues that were susceptible or resistant to cisplatin using quantitative real-time PCR. We also conducted in vitro and in vivo assays examining the function and mechanism of lnc-LBCSs. Knockdown of circSnx12 rendered cisplatin-resistant OC cells more sensitive to cisplatin in vitro and in vivo by activating ferroptosis, which was at least partially abolished by downregulation of miR-194-5p. Molecular mechanics studies indicate that circSnx12 can be a molecular sponge of miR-194-5p, which targets SLC7A11. According to our findings, circSnx12 ameliorates cisplatin resistance by blocking ferroptosis via a miR-194-5p/SLC7A11 pathway. CircARNT2 may thus serve as an effective therapeutic target for overcoming cisplatin resistance in OC. [BMB Reports 2023; 56(3): 184-189].

NEAT1 Overexpression Indicates a Poor Prognosis and Induces Chemotherapy Resistance via the miR-491-5p/SOX3 Signaling Pathway in Ovarian Cancer.

BACKGROUND: Accumulated studies have reported that dysregulated long non-coding RNAs (lncRNAs) are crucial in ovarian cancer (OC) initiation and development. However, detailed biological functions of lncRNA NEAT1 during the progression of OC remains to be uncovered. PURPOSE: Our aim was to identify the role of NEAT1 in cisplatin resistance of ovarian cancer and the underlying mechanisms. METHODS: The expression patterns of NEAT1 in OC cell lines and tissue samples were identified by qRT-PCR. The cisplatin (DDP) sensitivity of OC cells was detected by MTT and CCK8 assay, while OC cell apoptosis and cell cycle were detected using flow cytometer assays. In addition, effects of NEAT1 on tumor growth were determined by xenograft tumor model. Luciferase reporter assay was conducted to prove the regulatory relation of miR-491-5p, NEAT1, and SOX3. Importantly, the expression of NEAT1 in exosomes from cisplatin-resistant patients was also determined by using qRT-PCR. RESULTS: In this study, upregulated NEAT1 was detected in OC cell lines and tissues. Meanwhile, NEAT1 was also increased in cisplatin-resistant OC cell lines and tissues. Upregulation of NEAT1 inhibited cisplatin-induced OC cell apoptosis and promoted cell proliferation, while knockdown of NEAT1 played the opposite role. These effects were also observed in vivo. Furthermore, direct interaction was observed between NEAT1 and miR-491-5p. NEAT1 led to the upregulation of miR-491-5p-targeted SOX3 mRNA. Importantly, this study also showed upregulated NEAT1 expression in serum exosomes derived from cisplatin-resistant patients. CONCLUSION: NEAT1 is vital in the chemoresistance of ovarian cancer through regulating miR-491-5p/SOX3 pathway, showing that NEAT1 might be a potential target for OC resistance treatment.

Effect of vitamin D on clinical and biochemical parameters in polycystic ovary syndrome women: A meta-analysis.

AIM: Using a meta-analysis framework, we investigated the association between the serum level of vitamin D and the risk of polycystic ovary syndrome (PCOS) and further examined the therapeutic effect of vitamin D on the clinical features of PCOS. MATERIAL AND METHODS: Multiple databases were searched to retrieve studies. We chose clinical studies that investigated the relation between the serum level of vitamin D and the risk of PCOS or the therapeutic effect of vitamin D on PCOS. The search results were screened according to strict inclusion and exclusion criteria to select high-quality studies for inclusion. Statistical analyses were carried out using stata 12.0. RESULTS: Seventeen studies were eligible in this meta-analysis. The levels of 25-hydroxyvitamin D and the quantitative insulin-sensitivity check index in the PCOS group were remarkably lower than in the controls, whereas the homeostasis model assessment of insulin resistance in the PCOS group was markedly higher than in the controls. No statistically significant difference was observed in serum parathyroid hormone levels between the two groups. The 25-hydroxyvitamin D levels were significantly elevated after PCOS patients received vitamin D3 treatment, but serum parathyroid hormone concentration, homeostasis model assessment of insulin resistance and quantitative insulin-sensitivity check index did not show any significant changes, indicating a lack of therapeutic response. CONCLUSION: Our results suggest that the serum level of vitamin D is associated with the risk of PCOS, but the therapeutic effect of vitamin D on PCOS remains to be further explored.