SOX9‐activated PXN‐AS1 promotes the tumorigenesis of glioblastoma by EZH2‐mediated methylation of DKK1

Chen, Hongjin; Hou, Guanyu; Yang, Jian; Chen, Weilin; Guo, Liemei; Qin, Mei; Ge, Jian; Zhang, Xiaohua

doi:10.1111/jcmm.15189

Cited by 21 publications

(13 citation statements)

References 35 publications

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“…Glioblastoma cells show elevated levels of LncRNA PXN-AS1. Apoptosis of glioblastoma cells was promoted by PXN-AS1 inhibition through lowering Bcl-2 and elevating Bax ( Chen et al, 2020 ). There are low levels of TAF15 and LncRNA LINC00665 in glioma, on the contrary, high levels of MTF1, YY2, and GTSE1 are observed.…”

Section: Non-coding Rnas and Brain Tumorsmentioning

confidence: 99%

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Non-Coding RNAs and Brain Tumors: Insights Into Their Roles in Apoptosis

Tamtaji

Derakhshan

Noshabad

et al. 2022

Front. Cell Dev. Biol.

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A major terrifying ailment afflicting the humans throughout the world is brain tumor, which causes a lot of mortality among pediatric and adult solid tumors. Several major barriers to the treatment and diagnosis of the brain tumors are the specific micro-environmental and cell-intrinsic features of neural tissues. Absence of the nutrients and hypoxia trigger the cells’ mortality in the core of the tumors of humans’ brains: however, type of the cells’ mortality, including apoptosis or necrosis, has been not found obviously. Current studies have emphasized the non-coding RNAs (ncRNAs) since their crucial impacts on carcinogenesis have been discovered. Several investigations suggest the essential contribution of such molecules in the development of brain tumors and the respective roles in apoptosis. Herein, we summarize the apoptosis-related non-coding RNAs in brain tumors.

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Section: Non-coding Rnas and Brain Tumorsmentioning

confidence: 99%

“…Glioblastoma cells show elevated levels of LncRNA PXN-AS1. Apoptosis of glioblastoma cells was promoted by PXN-AS1 inhibition through lowering Bcl-2 and elevating Bax (Chen et al, 2020).…”

Section: Long Non-coding Rnas and Apoptosis In Brain Tumorsmentioning

confidence: 99%

Non-Coding RNAs and Brain Tumors: Insights Into Their Roles in Apoptosis

Tamtaji

Derakhshan

Noshabad

et al. 2022

Front. Cell Dev. Biol.

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“…Enhancer of zeste homologue 2 (EZH2) is a key member of the polycomb group genes and is able to promote the malignancy of cancer cells via inhibiting the expression of a variety of tumor suppressor genes (TSGs) [330]. EZH2 dually enhances the migration and proliferation of cancer cells, and targeting this oncogene factor is a promising strategy in cancer therapy [331,332]. In GC cells, STAT3 functions as an upstream mediator of EZH2.…”

Section: Stat3 As An Oncogene Factor In Gastric Cancermentioning

confidence: 99%

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

Ashrafizadeh

Zarrabi

Orouei

et al. 2020

Biology

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Molecular signaling pathways play a significant role in the regulation of biological mechanisms, and their abnormal expression can provide the conditions for cancer development. The signal transducer and activator of transcription 3 (STAT3) is a key member of the STAT proteins and its oncogene role in cancer has been shown. STAT3 is able to promote the proliferation and invasion of cancer cells and induces chemoresistance. Different downstream targets of STAT3 have been identified in cancer and it has also been shown that microRNA (miR), long non-coding RNA (lncRNA) and other molecular pathways are able to function as upstream mediators of STAT3 in cancer. In the present review, we focus on the role and regulation of STAT3 in gastric cancer (GC). miRs and lncRNAs are considered as potential upstream mediators of STAT3 and they are able to affect STAT3 expression in exerting their oncogene or onco-suppressor role in GC cells. Anti-tumor compounds suppress the STAT3 signaling pathway to restrict the proliferation and malignant behavior of GC cells. Other molecular pathways, such as sirtuin, stathmin and so on, can act as upstream mediators of STAT3 in GC. Notably, the components of the tumor microenvironment that are capable of targeting STAT3 in GC, such as fibroblasts and macrophages, are discussed in this review. Finally, we demonstrate that STAT3 can target oncogene factors to enhance the proliferation and metastasis of GC cells.

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“…In melanoma cell lines, EZH2 is the only functional protein that binds to LINC-PINT in the nuclei, and LINC-PINT exerts an inhibitory effect on the pathogenesis of melanoma through enriching EZH2 to the promoter of its target genes [15]. Moreover, an evidence suggested that EZH2 mediates tumor progressions through regulating the expression levels of multiple genes, including KLF2, DKK-1, CDKN1C, ZEB1, ACE2, Robo4, P4HA1, and DUXAP8 [16][17][18][19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC-PINT Inhibits Malignant Behaviors of Laryngeal Squamous Cell Carcinoma Cells via Inhibiting ZEB1

Yang¹,

Miao²,

Mao³

et al. 2021

Pathol. Oncol. Res.

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Objective: Laryngeal squamous cell carcinoma (LSCC) belongs to head and neck squamous cell carcinoma (HNSCC), with dismal prognosis. Here, this study aims to disclose the role of LINC-PINT in cancer development, which may contribute to improving the clinical outcomes of LSCC treatment.Methods: LINC-PINT expression in LSCC tissues and in TU-177 and Hep-2 cells was quantified, and subsequently, the association between LINC-PINT and LSCC malignancies was analyzed. pcDNA3.1-LINC-PINT or pcDNA3.1-EZH2 was introduced into Hep-2 and TU-177 cells. qRT-PCR and Western blot analyses examined the levels of proteins related to the AKT/mTOR pathway and their phosphorylated proteins in Hep-2 and TU-177 cells. The viability as well as migration and invasion abilities of Hep-2 and TU-177 cells were determined. Also, the distribution of LINC-PINT in Hep-2 cells was investigated as well as the interplay between LINC-PINT and EZH2. The downstream genes that might interact with EZH2 were screened.Results: LINC-PINT expression was inhibited in LSCC tissues and in Hep-2 and TU-177 cells, whose downregulation was associated with unsatisfactory prognosis. LINC-PINT overexpression suppressed the proliferative, migratory and invasive capacities of Hep-2 and TU-177 cells. LINC-PINT, mainly expressing in nuclei, could enrich EZH2 to silence ZEB1. In Hep-2 and TU-177 cells, the inhibition of LINC-PINT or overexpression of ZEB1 could enhance cell proliferation, migration and invasion. The phosphorylated levels of proteins related to the AKT/mTOR pathway were declined in cells with LINC-PINT overexpression, and the levels of these phosphorylated proteins were increased in cells with LINC-PINT inhibition.Conclusion: LINC-PINT enriches EZH2 to silence ZEB1 and thus inhibits the proliferative, migratory, and invasive capacities of Hep-2 and TU-177 cells. In addition, LINC-PINT might exert its biological function through the AKT/mTOR pathway.

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SOX9‐activated PXN‐AS1 promotes the tumorigenesis of glioblastoma by EZH2‐mediated methylation of DKK1

Cited by 21 publications

References 35 publications

Non-Coding RNAs and Brain Tumors: Insights Into Their Roles in Apoptosis

Non-Coding RNAs and Brain Tumors: Insights Into Their Roles in Apoptosis

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

LncRNA LINC-PINT Inhibits Malignant Behaviors of Laryngeal Squamous Cell Carcinoma Cells via Inhibiting ZEB1

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