lncRNA KCNQ1OT1 promotes proliferation and invasion of glioma cells by targeting the miR‑375/YAP pathway

Ding, Panfeng; Liang, Bo; Shou, Jixin; Wang, Xinjun

doi:10.3892/ijmm.2020.4760

Cited by 12 publications

(6 citation statements)

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“…Another study shown that lncRNA KCNQ1OT1 promotes proliferation and invasion of glioma cells by targeting the miR-375/YAP pathway. The results indicated that KCNQ1OT1 was upregulated in glioma tissues compared with adjacent tissues, which was associated with poor prognosis (Ding et al, 2020).…”

Section: Mirna-long Non-coding Rna Interaction In Glioma: Research Ou...mentioning

confidence: 99%

Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

Wei

et al. 2022

Front. Mol. Neurosci.

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As is known to all, glioma, a global difficult problem, has a high malignant degree, high recurrence rate and poor prognosis. We analyzed and summarized signal pathway of the Hippo/YAP, PI3K/AKT/mTOR, miRNA, WNT/β-catenin, Notch, Hedgehog, TGF-β, TCS/mTORC1 signal pathway, JAK/STAT signal pathway, MAPK signaling pathway, the relationship between BBB and signal pathways and the mechanism of key enzymes in glioma. It is concluded that Yap1 inhibitor may become an effective target for the treatment of glioma in the near future through efforts of generation after generation. Inhibiting PI3K/Akt/mTOR, Shh, Wnt/β-Catenin, and HIF-1α can reduce the migration ability and drug resistance of tumor cells to improve the prognosis of glioma. The analysis shows that Notch1 and Sox2 have a positive feedback regulation mechanism, and Notch4 predicts the malignant degree of glioma. In this way, notch cannot only be treated for glioma stem cells in clinic, but also be used as an evaluation index to evaluate the prognosis, and provide an exploratory attempt for the direction of glioma treatment. MiRNA plays an important role in diagnosis, and in the treatment of glioma, VPS25, KCNQ1OT1, KB-1460A1.5, and CKAP4 are promising prognostic indicators and a potential therapeutic targets for glioma, meanwhile, Rheb is also a potent activator of Signaling cross-talk etc. It is believed that these studies will help us to have a deeper understanding of glioma, so that we will find new and better treatment schemes to gradually conquer the problem of glioma.

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Section: Mirna-long Non-coding Rna Interaction In Glioma: Research Ou...mentioning

confidence: 99%

Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

Wei

et al. 2022

Front. Mol. Neurosci.

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“…It was recently documented that miR-375 was expressed at low levels in glioma, and inhibited tumor growth and cancer cell proliferation (59). miR-375 has been reported to function in regulating glioma cell proliferation, with the addition of the miR-375 inhibitor enhancing cell proliferation in both U251MG and U87-MG cells (60). miR-375 is a multi-functional regulator in a diverse range of cellular pathways, which can regulate numerous functional genes (61).…”

Section: Discussionmentioning

confidence: 99%

Silencing long noncoding RNA LINC01138 inhibits aerobic glycolysis to reduce glioma cell proliferation by regulating the microRNA‑375/SP1 axis

Yin

Jiang

et al. 2021

Mol Med Rep

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Glioma is a primary cerebral neoplasm that originates from glial tissue and spreads to the central nervous system. Long noncoding RNAs are known to play a role in glioma cells by regulating cell proliferation, migration and invasion. The aim of the present study was to investigate the mechanism by which long intergenic non-protein coding RNA (LINC) 01138 affects glycolysis and proliferation in glioma cells via the microRNA (miR)-375/specificity protein 1 (SP1) axis. LINC01138 expression was assessed in glioma tissues and cells using reverse transcription-quantitative PCR and the association between LINC01138 and patient clinicopathological features was analyzed. Glucose uptake, lactic acid secretion, cell proliferation, and glycolysis-related enzyme levels were detected following LINC01138 silencing using CCK-8, EDU assay and western blot analysis. miR-375 and SP1 expression levels were also assessed, and the distribution of LINC01138 in the nucleus and cytoplasm was investigated using subcellular fractionation localization. Furthermore, the binding relationships between LINC01138 and miR-375, and between miR-375 and SP1 were assessed via dual-luciferase experiment, RIP and RNA pull-down assays. Finally, xenograft transplantation models were used to verify the in vitro results. LINC01138 was highly expressed in glioma, which was independent of patient sex or age but was significantly related to tumor diameter, the World Health Organization tumor grade and lymph node metastasis. Silencing LINC01138 significantly reduced glioma glycolysis and cell proliferation. Moreover, LINC01138 acted as a competing endogenous RNA to sponge miR-375 and promote SP1 expression. miR-375 inhibition significantly reversed the effect of LINC01138 silencing. In addition, silencing LINC01138 significantly reduced tumor growth in vivo. The present study demonstrated that silencing LINC01138 inhibited aerobic glycolysis and thus reduced glioma cell proliferation, potentially by modulating the miR-375/SP1 axis.

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“…Evidence has showed that KCNQ1OT1 can promote cell proliferation and migration [40]. KCNQ1OT1 was found to enhance glioma cell proliferation and invasion via regulating the miR-375/YAP pathway and thereby accelerated the progression of glioma [41]. Meanwhile, in colorectal cancer, KCNQ1OT1 can induce cell apoptosis by sponging miR-329-3p [42].…”

Section: Discussionmentioning

confidence: 99%

LncRNA-KCNQ1OT1: A Potential Target in Exosomes Derived From ADSCs for The Treatment of Osteoporosis

Wang

Jia²,

Chen

2021

Preprint

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Background Osteoporosis is a worldwide medical and socioeconomic threat characterized by systemic impairment to bone strength and microstructure. Exosomes derived from adipose-derived stem cells (ADSCs-Exos) have been confirmed to play effective roles in the repair of various tissues and organs. This study aimed to investigate the role of ADSCs-Exos and a noval long none coding RNAKCNQ1OT1 (lnc-KCNQ1OT1) played in osteoporosis as well as the underlying mechanism. Methods MC3T3-E1 cells were treated with different doses of TNF-α (0, 1, 2.5, 5, 10 ng/ml) and then co-cultured with ADSCs-Exos or exosomes-derived from lnc-KCNQ1OT1-modified ADSCs (KCNQ1OT1-Exos). The expression of microRNA (miRNA)-141-5p (miR-141-5p) and lnc-KCNQ1OT1 was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of cleaved-caspase-3, caspase-3 and Bax was determined by Western blot. Cell viability and apoptosis were assessed by cell counting kit 8 (CCK-8) and flow cytometry analysis, respectively. The binding sites between KCNQ1OT1 and miR-141-5p were validated by dual-luciferase reporter assay. Results Tumor necrosis factor-α (TNF-α) dose dependently increased miR-141-5p expression, inhibited viability and promoted apoptosis of MC3T3-E1 cells. However, miR-141-5p silencing or co-culture with ADSCs-Exos attenuated these effects. In addition, KCNQ1OT1-Exos could more significantly attenuate the induced cytotoxicity and apoptosis compared to ADSCs-Exos. Moreover, miR-141-5p was confirmed as the target of lnc-KCNQ1OT1 by luciferase reporter assay. Conclusions ADSCs-Exos attenuated cytotoxicity and apoptosis of TNF-α-induced MC3T3-E1 cells. KCNQ1OT1-Exos had a more significant inhibitory effect compared to ADSCs-Exos by the function of sponging miR-141-5p, suggesting that KCNQ1OT1-Exos could be promising agents in osteoporosis treatment.

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lncRNA KCNQ1OT1 promotes proliferation and invasion of glioma cells by targeting the miR‑375/YAP pathway

Cited by 12 publications

References 50 publications

Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

Silencing long noncoding RNA LINC01138 inhibits aerobic glycolysis to reduce glioma cell proliferation by regulating the microRNA‑375/SP1 axis

LncRNA-KCNQ1OT1: A Potential Target in Exosomes Derived From ADSCs for The Treatment of Osteoporosis

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