XIST promotes cell proliferation and invasion by regulating miR-140-5p and SOX4 in retinoblastoma

Wang, Yuhui; Sun, Dahong; Sheng, Ying; Guo, Hong; Meng, Fan-Chun; Song, Tingting

doi:10.1186/s12957-020-01825-8

Cited by 16 publications

(7 citation statements)

References 31 publications

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“…miR‐338‐3p can suppress lung cancer by targeting SOX4 (Y. Li et al, ). miR‐211 can inhibit gastric cancer progression by targeting SOX4 (C. Y. Wang et al, ). miR‐132 can inhibit cell growth in osteosarcoma by targeting Sox4 (Liu, Li, Liu, Wu, & Zhu, ).…”

Section: Discussionmentioning

confidence: 99%

Involvement of NEAT1/miR‐133a axis in promoting cervical cancer progression via targeting SOX4

Yuan

Zhou

et al. 2019

Journal Cellular Physiology

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NEAT1 is an important tumor oncogenic gene in various tumors. Nevertheless, its involvement remains poorly studied in cervical cancer. Our study explored the functional mechanism of NEAT1 in cervical cancer. NEAT1 level in several cervical cancer cells was quantified and we found NEAT1 was greatly upregulated in vitro. NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis. For another, microRNA (miR)‐133a was downregulated in cervical cancer cells and NEAT1 negatively modulated miR‐133a expression. Subsequently, we validated that miR‐133a functioned as a potential target of NEAT1. Meanwhile, SOX4 is abnormally expressed in various cancers. SOX4 was able to act as a downstream target of miR‐133a and silencing of SOX4 can restrain cervical cancer progression. In addition, in vivo assays were conducted to prove the role of NEAT1/miR‐133a/SOX4 axis in cervical cancer. These findings implied that NEAT1 served as a competing endogenous RNA to sponge miR‐133a and regulate SOX4 in cervical cancer pathogenesis. To sum up, it was implied that NEAT1/miR‐133a/SOX4 axis was involved in cervical cancer development.

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Section: Discussionmentioning

confidence: 99%

Involvement of NEAT1/miR‐133a axis in promoting cervical cancer progression via targeting SOX4

Yuan

Zhou

et al. 2019

Journal Cellular Physiology

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“…For example, lncRNA PLAC2 induced RB cell apoptosis via regulating PTEN expression [ 24 ]. Knockdown of lncRNA XIST repressed the proliferation and invasion of RB cells by miR-140-5p/SOX4 signaling [ 25 ]. And lncRNA TP73-AS1 activated TFAP2B-mediated cell proliferation, metastasis, and invasion in RB via decoying miRNA-874-3p [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

KCNQ1OT1 regulates the retinoblastoma cell proliferation, migration and SIRT1/JNK signaling pathway by targeting miR-124/SP1 axis

Zhang

Yang

et al. 2021

Bioscience Reports

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Objective: Long non-coding RNA (lncRNA) KCNQ1OT1 was reported to be tightly associated with tumorigenesis and progression of multiple cancers. However, the expression and biological functions of KCNQ1OT1 in retinoblastoma (RB) are still unknown. We aim to elucidate the potential function and underlying mechanism of KCNQ1OT1 in regulating the progression of RB. Methods: The levels of KCNQ1OT1 were assayed by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) analysis. The cell proliferation of RB cells (Y79 and WERI-Rb-1) were evaluated through Cell Counting Kit 8 (CCK-8) assay. Meanwhile, Y79 and WERI-Rb-1 cell apoptosis and cell cycle were assessed by Flow Cytometry analysis. Dual luciferase reporter assay were performed to illustrate the interaction between KCNQ1OT1, miR-124, and SP1. Results: We found that KCNQ1OT1 was up-regulated and miR-124 was down-regulated in RB tissues and cells. Moreover, knockdown of KCNQ1OT1 reduced the proliferation, migration, and cell cycle, as well as promoted cell apoptosis of Y79 and WERI-Rb-1 cells. Western blot analysis consistently proved cell cycle and apoptosis related protein expression levels. More importantly, KCNQ1OT1 was a sponge of microRNA (miR)-124. MiR-124 inhibition strongly reversed the effect on cell proliferation, cycle arrest, and apoptosis by KCNQ1OT1 knockdown mediation. In addition, KCNQ1OT1 regulated expression of SP1, a direct target of miR-124 in RB. On the other hand, miR-124 inhibitor abrogated the active effect of KCNQ1OT1 silencing on silent information regulator 1 (SIRT1)/c-Jun N-terminal kinase (JNK) signaling pathway. The function of KCNQ1OT1 was verified in vivo. Conclusions: These findings implied that KCNQ1OT1 silencing inhibited RB progression and activated SIRT1/JNK signaling pathway partially by modulating the miR-124/SP1 axis.

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“…et al, 2018;Li C. et al, 2018;Wang et al, 2018cWang et al, , 2019cLiu et al, 2019b;Qiu et al, 2019;Tian et al, 2019;Zhou et al, 2019e;Jiang et al, 2020;Rong et al, 2020;Xu et al, 2020 Osteosarcoma miR-21-5p, miR-193-3p, miR-195-5p, miR-137, miR-302b, miR-375-3p, miR-153 p21, NF-kB, PUMA, PDCD4, RSf1, YAP, RAP2B, AKT, mTOR, SNAl1 Wu D.P. et al, 2017;Zhang and Xia, 2017;Lv et al, 2018;Yang C. et al, 2018;Li H. et al, 2019;Sun X. et al, 2019;Wen et al, 2020 Pancreatic cancer miR-133a, miR-140, miR-124, miR-34a-5p, miR-34a, miR-141-3p, miR-429 EGFR, iASPP, YAP, EGFR, TGF-β2, ZEB1 Liang et al, 2017;Shen et al, 2019;Sun and Zhang, 2019;Zou et al, 2020 (Continued) Hu et al, 2018;Cheng Y. et al, 2019;Dong et al, 2020;Wang et al, 2020c;Zhao H. et al, 2020 Cervical cancer miR-200a, miR-140-5p, miR-889-3p Fus, ORC1, SIX1 Zhu H. et al, 2018;Chen X. et al, 2019c;Liu et al, 2020d Gastric cancer miR-101, miR-497, miR-185, miR-337 Chen D.L. et al, 2016;Zhang Q. et al, 2018;Zheng W. et al, 2020 1 protein (BRCA1) is a tumor suppressor.…”

Section: Lncrna Xist In Breast Cancermentioning

confidence: 99%

“…LncRNA Xist overexpression promotes retinoblastoma cells proliferation, migration, and invasion rates via negatively regulating lncRNA NKILA, but the causality has not been fully validated. In addition, lncRNA Xist, which indirectly interacts with miR-21-5p, miR-124, miR-101, miR-140-5p, and miR-200a-3p, and positively regulates VEGF, STAT3, ZEB1 and ZEB2, SOX4, and NRP1 expression, facilitates apoptosis, migration, EMT, proliferation, and invasion by activating signaling pathways, such as PI3K-Akt signaling pathway and MAPK-ERK signaling pathway ( Hu et al, 2018 ; Cheng Y. et al, 2019 ; Dong et al, 2020 ; Wang et al, 2020c ; Zhao H. et al, 2020 ). All in all, these studies suggested that lncRNA Xist serves a potential and promising clinical application for diagnosis, prognosis, and treatment.…”

Section: The Role Of Lncrna Xist In Cancermentioning

confidence: 99%

Biological Function of Long Non-coding RNA (LncRNA) Xist

Wang

Min

Guo

et al. 2021

Front. Cell Dev. Biol.

139

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Long non-coding RNAs (lncRNAs) regulate gene expression in a variety of ways at epigenetic, chromatin remodeling, transcriptional, and translational levels. Accumulating evidence suggests that lncRNA X-inactive specific transcript (lncRNA Xist) serves as an important regulator of cell growth and development. Despites its original roles in X-chromosome dosage compensation, lncRNA Xist also participates in the development of tumor and other human diseases by functioning as a competing endogenous RNA (ceRNA). In this review, we comprehensively summarized recent progress in understanding the cellular functions of lncRNA Xist in mammalian cells and discussed current knowledge regarding the ceRNA network of lncRNA Xist in various diseases. Long non-coding RNAs (lncRNAs) are transcripts that are more than 200 nt in length and without an apparent protein-coding capacity (Furlan and Rougeulle, 2016; Maduro et al., 2016). These RNAs are believed to be transcribed by the approximately 98–99% non-coding regions of the human genome (Derrien et al., 2012; Fu, 2014; Montalbano et al., 2017; Slack and Chinnaiyan, 2019), as well as a large variety of genomic regions, such as exonic, tronic, and intergenic regions. Hence, lncRNAs are also divided into eight categories: Intergenic lncRNAs, Intronic lncRNAs, Enhancer lncRNAs, Promoter lncRNAs, Natural antisense/sense lncRNAs, Small nucleolar RNA-ended lncRNAs (sno-lncRNAs), Bidirectional lncRNAs, and non-poly(A) lncRNAs (Ma et al., 2013; Devaux et al., 2015; St Laurent et al., 2015; Chen, 2016; Quinn and Chang, 2016; Richard and Eichhorn, 2018; Connerty et al., 2020). A range of evidence has suggested that lncRNAs function as key regulators in crucial cellular functions, including proliferation, differentiation, apoptosis, migration, and invasion, by regulating the expression level of target genes via epigenomic, transcriptional, or post-transcriptional approaches (Cao et al., 2018). Moreover, lncRNAs detected in body fluids were also believed to serve as potential biomarkers for the diagnosis, prognosis, and monitoring of disease progression, and act as novel and potential drug targets for therapeutic exploitation in human disease (Jiang W. et al., 2018; Zhou et al., 2019a). Long non-coding RNA X-inactive specific transcript (lncRNA Xist) are a set of 15,000–20,000 nt sequences localized in the X chromosome inactivation center (XIC) of chromosome Xq13.2 (Brown et al., 1992; Debrand et al., 1998; Kay, 1998; Lee et al., 2013; da Rocha and Heard, 2017; Yang Z. et al., 2018; Brockdorff, 2019). Previous studies have indicated that lncRNA Xist regulate X chromosome inactivation (XCI), resulting in the inheritable silencing of one of the X-chromosomes during female cell development. Also, it serves a vital regulatory function in the whole spectrum of human disease (notably cancer) and can be used as a novel diagnostic and prognostic biomarker and as a potential therapeutic target for human disease in the clinic (Liu et al., 2018b; Deng et al., 2019; Dinescu et al., 2019; Mutzel and Schulz, 2020; Patrat et al., 2020; Wang et al., 2020a). In particular, lncRNA Xist have been demonstrated to be involved in the development of multiple types of tumors including brain tumor, Leukemia, lung cancer, breast cancer, and liver cancer, with the prominent examples outlined in Table 1. It was also believed that lncRNA Xist (Chaligne and Heard, 2014; Yang Z. et al., 2018) contributed to other diseases, such as pulmonary fibrosis, inflammation, neuropathic pain, cardiomyocyte hypertrophy, and osteoarthritis chondrocytes, and more specific details can be found in Table 2. This review summarizes the current knowledge on the regulatory mechanisms of lncRNA Xist on both chromosome dosage compensation and pathogenesis (especially cancer) processes, with a focus on the regulatory network of lncRNA Xist in human disease.

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XIST promotes cell proliferation and invasion by regulating miR-140-5p and SOX4 in retinoblastoma

Cited by 16 publications

References 31 publications

Involvement of NEAT1/miR‐133a axis in promoting cervical cancer progression via targeting SOX4

Involvement of NEAT1/miR‐133a axis in promoting cervical cancer progression via targeting SOX4

KCNQ1OT1 regulates the retinoblastoma cell proliferation, migration and SIRT1/JNK signaling pathway by targeting miR-124/SP1 axis

Biological Function of Long Non-coding RNA (LncRNA) Xist

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