New Findings What is the central question of this study?This study was designed to investigate the molecular mechanism and biological roles of long non‐coding RNA activated by transforming growth factor‐β (lncRNA ATB) in the progression of cervical cancer. What is the main finding and its importance?Our study provided new insight into the cross‐talk between lncRNA ATB, miR‐144 and ITGA6, shedding light on the therapy for cervical cancer. Abstract The present study was designed to investigate the molecular mechanism and biological roles of long non‐coding RNA activated by transforming growth factor‐β (lncRNA ATB) in the progression of cervical cancer. The expression levels of lncRNA ATB, miR‐144 and integrin α6 (ITGA6) were detected in human cervical cancer cell lines using quantitative real‐time PCR and western blotting. Cell viability was quantified by MTT assay at 12, 24, 36, 48 and 72 h after transfection, and cell invasion was determined by the Transwell migration assay. The association among lncRNA ATB, miR‐144 and ITGA6 was disclosed by a dual‐luciferase reporter assay. We found that lncRNA ATB was highly expressed in human cervical cancer cell lines. Further investigation indicated that lncRNA ATB functioned as a competitive endogenous RNA (ceRNA) for miR‐144 to promote cervical cancer cell proliferation and invasion. We demonstrated that ITGA6 was a direct target of miR‐144, and lncRNA ATB facilitated the proliferation and invasion of cervical cancer cells via the miR‐144/ITGA5 axis. In conclusion, the lncRNA ATB/miR‐144/ITGA6 axis might be a promising therapeutic target for cervical cancer.

Vascular endothelial growth factor A (VEGFA) gene has three alternative exons which results in multiple isoforms. VEGFA has been found overexpressed in patients with endometrial cancer, but the VEGFA expression pattern and how it is regulated are still unknown. The level of VEGFA transcripts and protein isoforms were detected by semi‐quantitative Polymerase chain reaction (PCR) and immunoblotting in 29 paired endometrial tumor and adjacent nontumor control tissues. The level of three alternative splicing related proteins: RBM5, RBM6, and RBM10 was determined by immunoblotting. The H3K27Ac level in RBM10 promoter region was detected by ChIP‐PCR. The RBM10 promoter region methylation level were quantified by methylation‐sensitive high resolution melting. VEGFA165a was overexpressed and VEGFA165b level was reduced in tumors. RBM10 level was reduced in tumors. RBM10 level was negatively correlated with VEGFA165a level and positively correlated with VEGFA165b level in tumors. Using HEC‐1‐A and RL95‐2 cells, we confirmed that VEGFA165a/b expressed pattern was controlled by RBM10. MALAT1 level was increased in tumors but not involved in VEGFA alternative splicing. Reduced H3K27Ac level and increased DNA methylation in the promoter region controlled RBM10 expression in tumors. VEGFA alternative splicing in endometrial cancer was regulated by RBM10, the expression of which was controlled by histone acetylation and DNA methylation.

Although the functions of long noncoding RNA (lncRNA) called FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) have been well studied in multiple human cancer types, its expression status and detailed roles in cervical cancer remain unknown and merit investigation. This study was aimed at assessing FOXD2-AS1 expression in cervical cancer and at determining its effects on the aggressive behavior of cervical cancer in vitro and in vivo. Expression of FOXD2-AS1 in cervical cancer tissues and cell lines was determined via reverse-transcription quantitative PCR. The effects of FOXD2-AS1 on cervical cancer cells were examined by a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-Htetrazolium bromide (MTT) assay, flow-cytometric analysis, migration and invasion assays, and an in vivo tumorigenicity assay. FOXD2-AS1 was found to be significantly upregulated in cervical cancer tissues and cell lines. High FOXD2-AS1 expression was notably linked with the Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and depth of cervical invasion in patients with cervical cancer. Kaplan-Meier survival analysis revealed significantly shorter overall survival of patients when the tumor expression of FOXD2-AS1 was higher in comparison with those in patients with lower FOXD2-AS1 expression. In vitro functional assays revealed that downregulation of FOXD2-AS1 led to suppression of proliferation, migration, and invasiveness as well as to the induction of apoptosis of cervical cancer cells. In addition, FOXD2-AS1 silencing hindered tumor growth in vivo. Mechanism investigation revealed that FOXD2-AS1 functioned as a molecular sponge of microRNA-760 (miR-760). Furthermore, hepatoma-derived growth factor (HDGF) was validated as a direct target gene of miR-760 in cervical cancer cells. Moreover, an miR-760 knockdown reversed the effects of FOXD2-AS1 silencing on cervical cancer cells. FOXD2-AS1 possesses significant oncogenic activity in cervical cancer progression; this activity is mediated by sponging

Numb is a conserved protein plays important roles in the development of cancer. Two Numb isoforms have been found produced by alternative splicing and play contrast roles in regulating cellular functions. It is reported that the expression of Numb long isoform (Numb‐L) was increased in various kinds of cancers, but in endometrial cancer, the condition is still unknown. The level of two Numb transcripts and protein isoforms were detected by semiquantitative polymerase chain reaction and immunoblotting in 47 paired endometrial tumor and adjacent non‐tumor control tissues. The level of three alternative splicing related proteins: RBM5, RBM6, and RBM10 was determined by immunoblotting. MiRNAs targeting RBM10 were predicted by bioinformatics tools and their interaction with RBM10 was confirmed by luciferase assay and immunoblotting. The function of miR‐335 in endometrial cancer was examined in xenograft mouse model. Numb‐L level was increased in tumors and negatively correlated with RBM10 protein level. RBM10 mRNA level was not significantly altered in endometrial tumors suggesting its expression may regulated by post transcriptional regulators such as miRNAs. We identified miR‐133a, miR‐133b, and miR‐335 directly target RBM10, but only miR‐335 level increased in tumors and negatively correlated with RBM10 protein level. miR‐335 overexpression promoted tumor growth by downregulating RBM10 and upregulating Numb‐L level in xenograft mouse model. miR‐335 overexpression promoted Numb‐L expression via targeting RBM10 in endometrial cancer, which may provide new biomarkers for EC diagnosis.

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Comprehensive Summary Efficient synthesis of polyester polyols with tunable molecular weight and microstructures from cyclic anhydride/epoxide mixtures by taking advantage of chain transfer reaction remains a great challenge, because most of the catalysts exhibit poor tolerance to chain transfer agent (CTA). In this contribution, we demonstrated that potassium acetate (KOAc) and 18‐crown‐6 (18‐C‐6) combination has great potential in the synthesis of diverse polyester polyols with controllable molecular weight and high‐end group fidelity. Compared with KOAc, KOAc/18‐C‐6 pair could induce a much faster chain transfer between the active and dormant chains, and thus produce polyester polyols with narrow and monomodal distribution. In addition, polyester polyols could be efficiently prepared in laboratory by using commercially available cyclic anhydride without further purification (containing about 2% diacid residual as CTA) with an extremely low catalyst loading ([catalyst pair] : [anhydride] : [epoxide] = 1 : 50000 : 250000, [catalyst pair] = 0.0004 mol%). KOAc/18‐C‐6 could also promote the self‐switchable copolymerization of cyclic anhydride/epoxide/cyclic ester mixtures. Ring‐ opening copolymerization of cyclic ester was initiated automatically after the full conversion of cyclic anhydride, finally producing polyester polyols with ABA‐type block structure.

cervical cancer is a malignancy that threatens female health. The present study aimed to investigate the role of transgelin 2 (TaGln2) in cervical cancer. reverse transcription-quantitative polymerase chain reaction and western blotting were conducted to detect the mrna and protein expression levels of particular factors in Hela cells. cell counting kit-8, wound healing and Transwell assays were conducted to determine cell viability, and migratory and invasive abilities, respectively. The results demonstrated that the expression levels of TaGln2 were decreased in cervical cancer tissues and were associated with the survival time of patients with cervical cancer. in addition, the expression of TaGln2 was significantly reduced in three cervical cancer cell lines (Hela, SiHa and c-33a) compared with in a normal cervical cell line. The present study also demonstrated that TaGln2 overexpression in Hela cells could inhibit cell viability, migration and invasion, and it was suggested that this may occur via upregulation of the expression levels of e-cadherin and inhibitor of nuclear factor κ-light-chain-enhancer of activated B cells (nF-κB) (iκB), and downregulation of c-X-c chemokine receptor type 4, matrix metalloproteinase (MMP)-2, MMP-9, p50 and transcription factor p65. in conclusion, TaGln2 was revealed to inhibit cell viability, and the migratory and invasive abilities of Hela cervical cancer cells via regulating the expression of metastasis-associated factors and the nF-κB signaling pathway. The present study proposed a novel target gene for the diagnosis, treatment and prognosis of cervical cancer.

Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies and primarily presents with hyperandrogenism. Although environmental factors and genetic factors are thought to be the major reason, there still exists a lot of questions need to be answered. High expression of C-terminal-binding protein 1 antisense (CTBP1-AS) was identified as an independent risk factor for PCOS; however, the molecular mechanism of CTBP1-AS in PCOS regulation is unknown. In the present study, the expression level of CTBP1-AS was found to be significantly upregulated in patients with PCOS compared with healthy control patients. CTBP1-AS knockdown was demonstrated to reduce the proliferation and promote the apoptosis of granulosa tumor cells in vitro . It was also identified that the two core catalytic subunits of Polycomb repressive complex 2 (enhancer of zeste homolog 2 and embryonic and ectoderm development protein) interacted with CTBP1-AS in primary granulosa cells and KGN cells. In addition, cryptotanshinone treatment was demonstrated to effectively downregulate CTBP1-AS expression level. Data from the present study suggested a pathophysiological role of CTBP1-AS in PCOS and may provide a new potential target for PCOS treatment.