The study of either miR‐153‐3p or MCL1 gene in ovarian carcinoma (OVC) has been reported; however, the interaction between miR‐153‐3p and MCL1 gene in OVC as well as the influence of their interaction on OVC progression has not been reported yet. Herein we intended to study the effects of miR‐153‐3p/MCL1 axis in OVC. Web‐based bioinformatics algorithms including DIANA TarBase 8.0, PicTar, and TargetScan Human 7.2 were used to predict the microRNAs (miRNAs) that could target MCL1 mRNA. Patient characteristics data collection and tissue sample immunohistochemical staining were used to determine the expression level of miR‐153‐3p and MCL1. We determined to unravel the effects of the pairing‐up of miR‐153‐3p and MCL1 mRNA in OVC cell lines (OVCAR3 cell line and A2780) and xenografts (immunodeficient(immunodeficient Rag−/− mice) using several methods including real‐time quantitative reverse transcription polymerase chain reaction, westernWestern blot, colony formation assay, wound healing assay, Transwell invasion assay, flow cytometry assay, and xenograft assay. These experiments were performed to study OVC cellular activities such as cell growth and death and so forth in vitro and in vivo. Plenty of miRNAs that can target MCL1 mRNA have been identified, and we have narrowed them down to miR‐153‐3p. MCL1 gene was found overexpressed in OVC tissues and OVC cell lines at RNA and protein levels, whereas miR‐153‐3p was found under‐expressed in OVC tissues and cells. miR‐153‐3p was found to target MCL1 mRNA and interfered OVC progression. The repression of MCL1 gene expression caused by either miR‐153‐3p or small interfering RNA technique led to significantly reduced OVC cell growth and invasion in vitro. Lastly, the engraftment of transfected human OVC cells into Rag−/− mice confirmed the in vitro results. MCL1 gene acts as a cancer facilitator in OVC. In this study, we revealed the role of miR‐153‐3p on OVC progression by targeting MCL1 gene. Our work could comprehend the current understanding of OVC progression and contribute to the underlying aggression mechanism of this cancer.
Numerous studies have revealed that cofilin-l (CFL1) is associated with cancer cell migration and invasion in various types of tumor tissues. We investigated the roles of CFL1 in vulvar squamous cell carcinoma (VSCC). CFL1 expression was detected in VSCC and normal vulvar tissues using immunohistochemistry and western blotting. The vulvar carcinoma SW962 cell line was transfected with CFL1 small interfering RNA (siRNA) and exposed to periplocoside. We then assessed changes in cell proliferation, apoptosis, invasion and metastasis. We detected changes in CFL1 mRNA and protein expression by RT-PCR and western blotting, and alterations in protein expression of various relevant molecules by western blotting. CFL1 expression was found to be significantly upregulated in the VSCC tissues compared with the normal vulvar tissues by immunohistochemistry and western blotting (P<0.05) and was positively correlated with International Federation of Gynecology and Obstetrics (FIGO) stage, differentiation and lymphatic metastasis (P<0.05). After CFL1 knockdown by siRNA transfection, SW962 cells exhibited a decrease in growth, G1 phase cell cycle arrest, induction of apoptotic, low invasion and metastasis, and disrupted lamellipodium formation. We found that the protein expression of Bcl-xL, cyclin A1, MMP2, MMP9 and STAT3 was decreased, while expression of Bax was increased. Periplocoside inhibited SW962 cell growth, promoted apoptosis, suppressed invasion and migration, and lamellipodium formation. Periplocoside exposure resulted in lower CFL1, Bcl-xL, cyclin A1, MMP2, MMP9 and STAT3 levels, but a higher Bax level compared with the control group. We demonstrated that abnormal CFL1 expression may affect vulvar carcinogenesis and subsequent progression. CFL1 silencing by siRNA significantly inhibited VSCC cell progression, which suggests that CFL1 is a potential therapeutic target for vulvar cancer. Periplocoside, which was utilized in the present study for the clinical treatment of vulvar cancer, showed strong antitumor effects by suppression of CFL1 expression.
Background The Eurasian Spoonbill (Platalea leucorodia) occurs throughout Eurasia and North and sub-Saharan Africa, with three recognized subspecies and six geographically distributed populations. However, in China, we knew almost nothing about migration routes, habitat use and effectiveness of current site protection measures for this species. Methods We deployed Global Positioning System/Global System for Mobile Communications (GPS/GSM) satellite trackers on 29 Eurasian Spoonbills captured in summer in Mongolia and northeastern China, to obtain complete migration routes data from 10 individuals from 19 complete migration episodes. Results Tracking data showed no geographical overlap during the annual cycle in Eurasian Spoonbills marked in the two main summering areas. Birds marked in the Naoli River Basin in Heilongjiang Province, China, wintered along the Jiangsu coastline in China, while Eurasian Spoonbills from two discrete summering areas (in Inner and western Mongolia) overwintered inland in the Yangtze River floodplain of China. Excluding the single Inner Mongolian bird, spring migration was significantly faster than autumn migration in the other two groups of birds. Eurasian Spoonbills mainly used water, wetland and grassland habitats in summer, but almost exclusively water in winter. Lack of protection of staging sites used by all the birds in spring and poor levels of protection throughout the annual cycle for western Mongolian birds (5–22%) gives considerable cause for concern, although sites used in other time by East Mongolian and Naoli River birds in the rest of their annual life cycle enjoyed good levels of protection (49–95%). Conclusions These results revealed previously unknown relationships between summering and wintering areas, migration routes and stopover sites for Eurasian Spoonbills wintering in China, suggesting the existence of discrete biogeographical population units. They also identified winter habitat use of Eurasian Spoonbills in China, confirming open water habitats as being critical throughout the annual cycle, although based on small sample size, gaps in current site safeguard networks for these populations.
Background Cisplatin resistance is a big challenge for ovarian cancer (OC) therapy. The abnormal expression of long noncoding RNAs (lncRNAs) regulated by N6‐methyladenosine (m6A) modification has been confirmed to play the crucial roles in OC. The aim of this study is to explore the regulatory mechanism of lncRNA RHPN1‐AS1 on OC with cisplatin resistance. Methods The real‐time reverse transcription‐polymerase chain reaction was carried out to confirm the expression of RHPN1‐AS1 and methyltransferase‐like 3 (METTL3) in OC. The effects of RHPN1‐AS1 on cisplatin‐resistant OC cells were identified by cell functional experiments and animal experiment. Western blotting was performed to detect the effect of RHPN1‐AS1 on PI3K/AKT pathway. Moreover, methylated RNA immunoprecipitation and RNA stability assays confirmed the interaction between RHPN1‐AS1 and METTL3. Results RHPN1‐AS1 and METTL3 were confirmed to be overexpressed in OC. After transfecting RHPN1‐AS1 overexpression or RHPN1‐AS1 knockdown vectors into cisplatin‐resistant OC cells, it was found that upregulating RHPN1‐AS1 contributed to cell viability, migration, invasion, and tumor growth in vivo. In addition, RHPN1‐AS1 could enhance the protein levels of PI3K and phosphorylated AKT in cisplatin‐resistant OC cells, and METTL3 could enhance the stability of RHPN1‐AS1 by the m6A modification. Conclusion Overall, this study revealed that METTL3‐mediated m6A modification of RHPN1‐AS1 accelerates cisplatin resistance in OC by activating PI3K/AKT pathway.
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