Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma

Fu, Zhenqiang; Luo, Wenzheng; Wang, Jingtao; Peng, Tao; Sun, Guifang; Shi, Jingyu; Li, Zhihong; Zhang, Boai

doi:10.1016/j.bbrc.2017.08.070

Cited by 89 publications

(65 citation statements)

References 25 publications

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“…microRNAs (miRNAs/miRs) have been reported to regulate certain ATGs at different stages of autophagy (40). Furthermore, the majority of lncRNAs serve a regulatory role by acting as sponges to sequester autophagy-associated miRNAs from their targets (41)(42)(43). Metastasis associated lung adenocarcinoma transcript 1 may upregulate the expression of the miR-101 targets stathmin 1, RAB5A, member RAS oncogene family and autophagy related 4D cysteine peptidase by acting as a sponge of miR-101, thus inducing autophagy (41).…”

Section: Autophagy and Its Regulationmentioning

confidence: 99%

“…Furthermore, the majority of lncRNAs serve a regulatory role by acting as sponges to sequester autophagy-associated miRNAs from their targets (41)(42)(43). Metastasis associated lung adenocarcinoma transcript 1 may upregulate the expression of the miR-101 targets stathmin 1, RAB5A, member RAS oncogene family and autophagy related 4D cysteine peptidase by acting as a sponge of miR-101, thus inducing autophagy (41). In anoxia/reoxygenation-induced autophagy of cardiomyocytes, the lncRNA autophagy promoting factor is upregulated to protect ATG7 from being degraded by miR-188-3p, and this promotes autophagic death of cardiomyocytes (42).…”

Section: Autophagy and Its Regulationmentioning

confidence: 99%

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Opportunities and challenges of co‑targeting epidermal growth factor receptor and autophagy signaling in non‑small cell lung cancer (Review)

Wang

et al. 2019

Oncol Lett

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Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are a standard therapy for patients with non-small cell lung cancer (NSCLC) with sensitive mutations. However, acquired resistance emerges following a median of 6-12 months. Several studies demonstrated that EGFR-TKI-induced tumor microenvironment stresses and autophagy are important causes of resistance. The current review summarizes the molecular mechanisms involved in EGFR-mediated regulation of autophagy. The role of autophagy in EGFR-TKI treatment, which may serve a role in protection or cell death, was discussed. Furthermore, co-inhibiting EGFR and autophagy signaling as a rational therapeutic strategy in the treatment of patients with NSCLC was explored. Contents 1. Introduction 2. EGFR and EGFR-TKI 3. Autophagy and its regulation 4. EGFR-mediated regulation of autophagy 5. Role of autophagy in EGFR-TKI treatment 6. Conclusions and perspectives

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Section: Autophagy and Its Regulationmentioning

confidence: 99%

Section: Autophagy and Its Regulationmentioning

confidence: 99%

Opportunities and challenges of co‑targeting epidermal growth factor receptor and autophagy signaling in non‑small cell lung cancer (Review)

Wang

et al. 2019

Oncol Lett

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“…Up to date, a number of lncRNAs have been received increased attention to participate in multiple major biological processes, including cellular homeostasis, development, differentiation, pluripotency of embryonic stem cells, and genomic imprinting . In addition, lots of evidence highlight that numbers of lncRNAs are well documented to be associated with human diseases and carcinogenesis, such as HOTAIR in hepatocellular carcinoma, lung cancer, breast cancer, and glioma . In fact, the aberrant level of lncRNAs has been well recognized as biomarkers for future cancer diagnostic, therapeutic, or prognostic …”

Section: Introductionmentioning

confidence: 99%

“…[10][11][12] In addition, lots of evidence highlight that numbers of lncRNAs are well documented to be associated with human diseases and carcinogenesis, such as HOTAIR in hepatocellular carcinoma, 13 lung cancer, 14 breast cancer, 15 and glioma. [16][17][18] In fact, the aberrant level of lncRNAs has been well recognized as biomarkers for future cancer diagnostic, therapeutic, or prognostic. 19,20 The underlying molecular mechanisms used by lncRNAs in intertwined gene regulatory network are complex and diverse.…”

mentioning

confidence: 99%

Long noncoding RNA HOXB13‐AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma

Xiong

Guo

et al. 2018

Cancer Medicine

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Dysregulation of long noncoding RNAs (lncRNAs) has been implicated in human diseases, in particular, cancers. In this study, we determined the expression of an lncRNA, HOXB13‐AS1, involving in glioma. We showed that HOXB13‐AS1 was significantly upregulated in glioma tissues and cells and was negatively correlated with its surrounding gene HOXB13 levels. Functional experiments in vitro and in vivo revealed that high level of HOXB13‐AS1 increased cell proliferation and tumor growth by promoting cell cycle progression. Conversely, knockdown of HOXB13‐AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13‐AS1 overexpression increased DNMT3B‐mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. Additionally, the interaction between HOXB13‐AS1 and HOXB13 was validated by RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays using antibody against to EZH2. Taken together, our study indicated that HOXB13‐AS1 could regulate HOXB13 gene expression by methylation HOXB13 promoter and acts as an epigenetic oncogenic in glioma.

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“…Their established risk score could distinguish the OS between the low-risk and high-risk groups, which was also validated using the TCGA dataset [19]. LncRNA MALAT1 activated autophagy and promoted cell proliferation of glioma cells by upregulating autophagy genes STMN1, RAB5A and ATG4D [46], while knockdown of MALAT1 inhibited cell migration and invasion of glioma cells by suppressing autophagy through regulation of autophagy gene GOLM1 [47]. Elevated lncRNA AC023115.3 and growth arrest-speci c 5 (GAS5) in human GBM cells were demonstrated to promote cisplatin-induced apoptosis by inhibiting autophagy [48,49].…”

Section: Discussionmentioning

confidence: 90%

Identification of an Autophagy-Related 10-lncRNA-mRNA Signature for Distinguishing Glioblastoma Multiforme from Lower‑Grade Glioma and Prognosis Prediction

Wei

Wang

Zhao

2020

Preprint

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Background: Autophagy provides the nutrients and energy for tumor growth, invasion and metastasis. Theoretically, autophagy-related mRNAs and regulatory long non-coding RNAs (lncRNAs) may represent promising biomarkers to predict tumor progression and poor prognosis. Our study aims to develop an autophagy-related signature to distinguish glioblastoma (GBM) from lower-grade gliomas (LGG) and predict overall survival (OS).Methods: The expression profile of GBM and LGG was collected from the Chinese Glioma Genome Atlas (CGGA) database that was used to identify differentially expressed genes (DEGs) and lncRNAs (DELs). The autophagy-related genes were obtained from the Human Autophagy Database. The autophagy-related DELs were identified by a co-expression network with DEGs. These DEGs and DELs underwent univariate and multivariate analyses to screen prognostic genes. They were entered into the Logit regression model to identify the GBM feature genes. The prognostic signature was evaluated by survival curve analyses and validated using The Cancer Genome Atlas (TCGA) dataset. The prognostic model and clinicopathological parameters were integrated to construct the nomogram.Results: A total of 131 autophagy-related DEGs and 54 autophagy-related DELs were identified. Ten of them were demonstrated as independent prognostic factors and could distinguish GBM from LGG, with the accuracy of 0.891 using CGGA dataset and 0.790 using TCGA dataset. The risk score was established based on these 10 genes. Patients with higher risk score were at an increased risk of developing GBM (49.7% vs 21.3%) and worse OS prognosis than those in low risk group. The predictive accuracy was 0.840 and 0.744 for CGGA and TCGA dataset, respectively. Multivariate analysis showed age, recurrence, IDH mutation and risk score status were independent prognostic factors and thus they were used to build a nomogram which showed the highest predictive power than other factors.Conclusion: The established nomogram may aid the clinical decision making of personalized treatment.

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Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma

Cited by 89 publications

References 25 publications

Opportunities and challenges of co‑targeting epidermal growth factor receptor and autophagy signaling in non‑small cell lung cancer (Review)

Opportunities and challenges of co‑targeting epidermal growth factor receptor and autophagy signaling in non‑small cell lung cancer (Review)

Long noncoding RNA HOXB13‐AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma

Identification of an Autophagy-Related 10-lncRNA-mRNA Signature for Distinguishing Glioblastoma Multiforme from Lower‑Grade Glioma and Prognosis Prediction

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