ABSTRACT. The objective of this study was to investigate the effect of downregulating long non-coding RNAs (lncRNAs) on the reversal of cisplatin resistance in CP70 ovarian cancer cells, and to identify the underlying mechanism(s) of action. An lncRNA microarray was performed to screen for downregulated lncRNAs in cisplatin-resistant CP70 cells. Expression levels of these lncRNAs were then verified in SKOV3 and SKOV3/DDP cells. Quantitative polymerase chain reaction was conducted to identify the lncRNA most downregulated, which was then synthesized and transfected into CP70 cells. To assess the viability and migration ability of these transfected CP70 cells, methyl thiazolyl tetrazolium and Transwell assays were carried out. In addition, expression levels of apoptosis-related proteins were examined by western blotting. The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. Transfection of lncRNA ENST00000457645 into CP70 cells markedly inhibited viability and migration ability, and significantly increased expression of apoptotic proteins such as Bax and cleaved caspase-3. lncRNA ENST00000457645 negatively affects the viability and migration of cisplatin-resistant CP70 ovarian cancer cells. The mechanism responsible involves modification of apoptotic protein expression.
Background It has been reported that miRNA-125b is associated with carcinogenesis and development of several different kinds of cancers. Nevertheless, there is no clarity regarding the significance and mechanism of action of miR-125b in clinical practice for cervical cancer (CC). Materials and methods In the current investigation, the expression of miR-125b in cervical clinical specimens and CC cell lines was analyzed via real-time quantitative PCR, and the relationship of miR-125b with the chromatin-associated protein high mobility group A (HMGA1) expression and clinicopathological parameters of CC patients was explored. Results The results indicated that miR-125b expression was remarkably upregulated in CC cell lines as well as in the tissues of humans. miR-125b overexpression was significantly related to a decrease in HMGA1 expression, progression-free survival, overall survival, and prognosis as well. Besides, knockdown of miR-125b inhibited proliferation and colony formation in SW756 and C4-1 cells, where the 3′-UTR of HMGA1 mRNA was directly targeted. Moreover, PI3K/Akt pathway was regulated by miR-125b through suppression of HMGA1. Conclusion These findings illustrated that a new regulatory role of HMGA1 is involved in the progression of CC. Our data demonstrated that miR-125b could play a critical role in the carcinogenesis and progression of CC, revealing that miR-125b might serve as a potential new target for treating CC.
Circular RNA (circRNA) is an endogenous RNA molecule with a stable closed-loop structure. The circular RNA HIPK3 (circHIPK3) is highly expressed in hepatocellular carcinoma and facilitates tumor growth. However, its role in cervical cancer (CC) and its regulatory mechanisms are not well-studied. This study aimed for investigating the function of circHIPK3 on proliferation and metastasis of CC cells. In this study, quantitative real-time PCR assay was adopted to delve into the circHIPK3 expression in CC cell lines. Cell counting kit-8 and colony formation assays were used to evaluate the influence of overexpression and knockdown of circHIPK3 on CC cell proliferation. Dual-luciferase reporter assay was employed to probe into the binding of miR-485-3p to circHIPK3 and miR-485-3p to the 3’ untranslated region (UTR) of fibroblast growth factor 2 (FGF2), respectively. FGF2 protein expression was detected by western blot analysis. This study confirmed that circHIPK3 was highly expressed in CC tissues. Overexpressed circHIPK3 could remarkably expedite the proliferation, migration and invasion of SiHa cells, and knocking down circHIPK3 could significantly impede the proliferation, migration and invasion of HeLa cells. MiR-485-3p can directly bind to circHIPK3 and the 3’UTR of FGF2. Overexpression of circHIPK3 triggered the upregulation of FGF2 expression while knockdown of circHIPK3 reduced FGF2 expression in CC cells, and the transfection of miR-485-3p mimics reversed the upregulation of FGF2 expression and enhanced malignant phenotypes in CC cells with overexpressed circHIPK3.
Polycystic ovary syndrome (PCOS) is a common female endocrine disorder that has a detriment impact on female health. Herein, the study used a case‐control analysis to sought to explore the association of rs13405728, rs12478601, and rs2479106 single nucleotide polymorphisms (SNPs) with in vitro fertilization and embryo transfer (IVF‐ET) efficacy in treating PCOS. A total of 163 PCOS patients (52 cycles) were selected as the PCOS group and 171 patients with tubal factor infertility without PCOS (68 cycles) were selected as the control group. Polymerase chain reaction was used to amplify genome DNA and direct sequencing to detect SNPs. The LHCGR rs13405728, THADA rs12478601, and DENND1A rs2479106 genotypes were subsequently tested. Logistic regression analysis was conducted to analyze the risk factors influencing the occurrence of PCOS as well as those influencing the efficacy of IVF‐ET. rs13405728, rs12478601, and family history of DM were influencing factors for the occurrence of PCOS. The rate of abortion and number of oocytes retrieved of patients with the THADA rs12478601 CC genotype increased but the rate of clinical gestation decreased. Patients with AG + GG genotype of the DENND1A rs2479106 had increased number of oocytes retrieved, rate of abortion and incidence of gestational DM. rs13405728, rs12478601, serum E2 value as well as fertility rate were influencing factors for efficacy of IVF‐ET. It was suggested that the TT genotype of LHCGR rs13405728, CC genotype of THADA rs12478601 and AG + GG genotype of DENND1A rs2479106 had poor outcomes of IVF‐ET in treating PCOS.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.