Abstract:Glioblastoma (GBM) recurrence is attributed to the presence of therapy‐resistant glioblastoma stem cells. Steroid receptor coactivator‐1 (SRC‐1) acts as an oncogenic regulator in many human tumors. The relationship between SRC‐1 and GBM has not yet been studied. Herein, we investigate the role of SRC‐1 in GBM. In this study, we found that SRC‐1 expression is positively correlated with grades of glioma and inversely correlated with glioma patient’s prognosis. Steroid receptor coactivator‐1 promotes the prolifer… Show more
“…This activity resulted in the inhibition of the proliferation, migration, and invasion of glioblastoma stem cells, and promoted their apoptosis (62). In line with Ma's study, recent research conducted by Gong showed that the miR-152/KLF4 axis enhanced the stemness of glioblastoma cells (63). The authors further discovered that the low expression of miR-152 was caused by activation of lncRNA X-inactive specific transcript (XIST) by steroid receptor coactivator-1 (SRC1).…”
The purpose of this study was to investigate the miRNAs and related mechanisms that regulates KLF4 in different cancers. Furthermore, we summarized the potential targets of miRNAs regulating the KLF4 pathway in cancer research.Background: MiRNAs are single-stranded, endogenous non-coding small RNAs, some of which are related to human cancers. miRNAs carry out post-transcriptional gene regulation through translation inhibition and degradation of target messenger RNAs (mRNAs) via complementarily pairing with their 3' untranslated regions. KLF4 is an important transcription factor with complex involvement in cancer.Increasing evidence shows that miRNAs are dysregulated in cancer and can regulate cancer-related signaling pathways, thereby affecting tumor progression.Methods: Systematic scientific literature searches were undertaken on PubMed using the following terms: "miRNAs and KLF4", "KLF4 and cancer", "miRNAs and cancer", and "miRNAs, KLF4 and cancer". Relevant papers were retrieved and further results were found by reviewing related papers and the references of the retrieved papers. We then conducted a narrative overview of the literature to summarize the results of the papers.
Conclusions:The role of KLF4 in cancer varies in a context-dependent manner. KLF4-regulating miRNAs in different tumors include miR-124
“…This activity resulted in the inhibition of the proliferation, migration, and invasion of glioblastoma stem cells, and promoted their apoptosis (62). In line with Ma's study, recent research conducted by Gong showed that the miR-152/KLF4 axis enhanced the stemness of glioblastoma cells (63). The authors further discovered that the low expression of miR-152 was caused by activation of lncRNA X-inactive specific transcript (XIST) by steroid receptor coactivator-1 (SRC1).…”
The purpose of this study was to investigate the miRNAs and related mechanisms that regulates KLF4 in different cancers. Furthermore, we summarized the potential targets of miRNAs regulating the KLF4 pathway in cancer research.Background: MiRNAs are single-stranded, endogenous non-coding small RNAs, some of which are related to human cancers. miRNAs carry out post-transcriptional gene regulation through translation inhibition and degradation of target messenger RNAs (mRNAs) via complementarily pairing with their 3' untranslated regions. KLF4 is an important transcription factor with complex involvement in cancer.Increasing evidence shows that miRNAs are dysregulated in cancer and can regulate cancer-related signaling pathways, thereby affecting tumor progression.Methods: Systematic scientific literature searches were undertaken on PubMed using the following terms: "miRNAs and KLF4", "KLF4 and cancer", "miRNAs and cancer", and "miRNAs, KLF4 and cancer". Relevant papers were retrieved and further results were found by reviewing related papers and the references of the retrieved papers. We then conducted a narrative overview of the literature to summarize the results of the papers.
Conclusions:The role of KLF4 in cancer varies in a context-dependent manner. KLF4-regulating miRNAs in different tumors include miR-124
“…Wang et al (42) have shown that KLF4 promotes spare respiratory capacity of human GBM cells by inducing mitochondrial fusion. Gong et al revealed that SRC-1 promotes GBM stemness through KLF4 activation (29). Wang et al found that HIF1/2a-induced KLF4 expression enhances the malignant progression of GBM by promoting stemness and cell cycle arrest (42).…”
Section: Discussionmentioning
confidence: 99%
“…KLF4 is a core component of the pluripotency transcription network that is involved in the regulation of cell cycle following DNA damage ( 28 ). A recent study has proved that KLF4 can be targeted by lncRNA XIST/miR-152 in regulating stemness in GBM ( 29 ). In this study, a screened prognosis-associated differentially expressed RNA (DER), CHRM3-AS2, was analysed in glioma.…”
ObjectivesLong non-coding RNAs (lncRNAs) are key regulators involved in the progression of glioma, and many functional lncRNAs are yet to be identified. This study aimed to explore the function of CHRM3-AS2, a rarely reported lncRNA, in glioma, as well as the underlying mechanisms involving miR-370-5p/KLF4.MethodsDifferentially expressed RNAs (DERs) were screened from two gene expression profiles of glioblastoma (GBM). Fluorescence in situ hybridisation was performed to determine the subcellular localisation of CHRM3-AS2. Cell viability, colony formation, apoptosis, migration, and invasion were evaluated using cell counting kit-8, colony counts, flow cytometry, wound healing, and Transwell assays, respectively. mRNA and protein expression of specific genes were measured using quantitative real-time polymerase chain reaction and western blotting, respectively. Dual luciferase reporter gene, RNA immunoprecipitation, and RNA pull-down assays were performed to identify the target relationships. A mouse xenograft model was established for in vivo validation.ResultsCHRM3-AS2 was screened as a prognosis-associated DER in GBM. CHRM3-AS2 expression was up-regulated in glioma cells, and CHRM3-AS2 was localised in the cytoplasm. Silencing of CHRM3-AS2 expression inhibited cell viability, colony formation, migration, and invasion and promoted apoptosis of U251 and SHG-44 cells. In addition, CHRM3-AS2 targeted miR-370-5p/KLF4 in glioma cells. The anti-tumour effect of CHRM3-AS2 silencing was weakened by miR-370-5p silencing or KLF4 overexpression. In vivo, silencing of CHRM3-AS2 expression inhibited tumour growth and Ki67 expression in mice. Overexpression of KLF4 also weakened the anti-tumour effect of CHRM3-AS2 silencing in mice.ConclusionsSilencing of CHRM3-AS2 expression inhibited the malignant progression of glioma by regulating miR-370-5p/KLF4 expression.
“…Additionally, SRC-1 was shown to elevate glioblastoma stemness by modulating the XIST/miR-152/KLF4 axis, which provided a new diagnostic and therapeutic biomarker for glioblastomas (Fig. 3 F) (Gong et al 2021 ). Fig.…”
Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is an important lncRNA derived from the XIST gene in mammals. XIST is abnormally expressed in numerous tumors, in most of which XIST functions as an oncogene. XIST is involved in multiple aspects of carcinogenesis, including tumor onset, progression, and prognosis. In our review, we collected and analyzed the recent studies on the impact of XIST in human tumor development. The multilevel molecular functions of XIST in human tumors are comprehensively reviewed to clarify the pathologic mechanisms and to offer a novel direction for further study.
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