LncRNA SNHG3 induces EMT and sorafenib resistance by modulating the miR‐128/CD151 pathway in hepatocellular carcinoma

Zhang, Peng-Fei; Wang, Fei; Wu, Jing; Wu, Yin; Huang, Wei; Liu, Dong; Huang, Xiaoyong; Zhang, Xuemei; Ke, Ai–Wu

doi:10.1002/jcp.27095

Cited by 158 publications

(143 citation statements)

References 21 publications

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“…SNHG3 was firstly implicated in Alzheimer's disease (AD) and its upregulation might be an indicator of a wider dysregulation of translational machinery and ribosome biogenesis during AD neurodegeneration [11]. Subsequently, it was revealed to be an oncogene and a biomarker of malignant status or poor prognosis in several types of cancers, including colorectal cancer, ovarian cancer and hepatocellular carcinoma [12][13][14]. However, no studies to date reported its potential tumor suppressor function in cancer.…”

Section: Introductionmentioning

confidence: 99%

lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

Duan¹,

Wang²,

Xu³

et al. 2020

J. Cancer

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The incidence of papillary thyroid carcinoma (PTC) has been increased rapidly in recent decades. Long noncoding RNAs (lncRNA) are a class of non-protein-coding transcripts and play critical roles in regulating gene expression and influence biological behaviors of multiple cancers, including PTC. Here, we discovered that lncRNA SNHG3 was significantly downregulated in PTC tissues and cell lines, the expression of SNHG3 was negatively correlated with the TNM stage and poor prognosis of PTC patients. Functional studies illustrated that the depletion of SNHG3 via CRISPR/Cas9 technology promoted the proliferation, migration and invasion abilities of PTC cells. Tumor xenograft models confirmed the tumor-promoting role of silenced SNHG3 in vivo. Further mechanistic analyses revealed that knockout of SNHG3 activated the AKT/mTOR/ERK pathway in PTC cell lines and the mTOR inhibitor AZD8055 abrogated the tumor-promoting effect induced by SNHG3 inhibition. Taken together, our findings identified a lncRNA SNHG3 that functions its tumor-suppressor role during PTC development and SNHG3 might serve as a promising candidate for target therapy of PTC.

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Section: Introductionmentioning

confidence: 99%

lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

Duan¹,

Wang²,

Xu³

et al. 2020

J. Cancer

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“…miRNAs are most frequently studied and some of them have been proved to be significantly dysregulated in HCC, promoting tumor progression and sorafenib resistance [83,84]. Consistent with the idea that certain cell states determine drug sensitivity, miRNAs, as well as other ncRNAs including lncRNAs that mostly act as sponges of miRNAs, modulated sorafenib sensitivity through regulating EMT and stemness in HCC [85]. There are no studies reporting the role of circular RNAs (circRNAs) in sorafenib resistance yet, however, circRNA was involved in regulating stemness features of HCC cells [86].…”

Section: Post-transcriptional Regulationmentioning

confidence: 84%

The microenvironmental and metabolic aspects of sorafenib resistance in hepatocellular carcinoma

et al. 2020

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A B S T R A C TIn most cases, sorafenib-resistant HCC cells exhibit significant mesenchymal phenotype and stemness features. In this context, tumor cells might undergo cell fate transition in response to sorafenib or other targeted drugs in the presence or absence of genetic mutations. Therefore, understanding the major characteristics of drug-resistant cells state helps to discover new treatments that overcome drug resistance. To note, little is known about the metabolic or microenvironmental aspects of the certain tumor cell states beyond the genome. This review mainly focuses on the underlying mechanisms of acquired sorafenib resistance based on CSCs and EMT models, which explain tumor heterogeneity and have been considered the major cause of secondary sorafenib resistance. In particular, it discusses how the tumor microenvironment and tumor metabolism regulate cell stemness, mesenchymal state, and sorafenib resistance through epigenetic regulations, and provides reliable targets that might have synergetic effect with sorafenib.

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“…So far, lots of lncRNAs have been con rmed to be involved in EMT. For example, lncTCF7 and SNHG3 can promote the progress of cancer through enhancing EMT in HCC 19,20 .…”

Section: Discussionmentioning

confidence: 99%

A Novel lncRNA loc339803 acts as CeRNA of miR-30a-5p to promote the migration and invasion of hepatocellular carcinoma cells

Xue

Zhang

Gao

et al. 2020

Preprint

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Background Hepatocellular carcinoma (HCC) is one of the most common malignant tumors, and has an unfavorable clinical outcome. Emerging evidences have demonstrated that long noncoding RNAs (lncRNAs) play an important role in the carcinogenesis and progression of HCC. However, the clinical significances, the biological roles of most lncRNAs in HCC remain poorly understood. Methods The expression levels of lncRNA loc339803 in HCC tissues and cell lines were determined by quantitative real-time polymerase chain reaction(qRT-PCR) assay. The cellular sublocalization of loc339803 were determined by fluorescence in situ hybridization and nuclear & cytoplasmic RNA isolation assay. Western blot, CCK-8, Edu, colony formation, migration and invasion assays were used to investigate the roles of loc339803 in progression of HCC in vitro. A mouse model for lung metastasis was constructed to evaluate the role of loc339803 in HCC development in vivo. The correlations among loc339803, miR-30a-5p and SNAIL1 were validated by qRT-PCR and a dual- luciferase reporter assay. Results The expression of loc339803 was upregulated in HCC tissues and cell lines, and positively correlated with tumor size, advanced tumor stage, higher serum AFP level and poor prognosis of HCC patients. loc339803 can promote the migration and invasion of HCC cells in vivo and in vitro. Further studies demonstrated the loc339803 functioned as a competing endogenous RNA (ceRNA) by directly binding to miR-30a-5p, thus up-regulating the expression of snai1, a target gene of miR-30a-5p. Moreover, miR-30a-5p upregulation blocked the enhancement of migration and invasion of HCC cells induced by loc339803 overexpression. Conclusions Loc339803 may be oncogenic in HCC and associated with poor clinical outcomes. LncRNA loc339803 might promote the invasion and migration of HCC cells through regulating miR-30a-5p/ SNAIL1 axis.

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LncRNA SNHG3 induces EMT and sorafenib resistance by modulating the miR‐128/CD151 pathway in hepatocellular carcinoma

Cited by 158 publications

References 21 publications

lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

The microenvironmental and metabolic aspects of sorafenib resistance in hepatocellular carcinoma

A Novel lncRNA loc339803 acts as CeRNA of miR-30a-5p to promote the migration and invasion of hepatocellular carcinoma cells

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