The Underlying Mechanisms of Noncoding RNAs in the Chemoresistance of Hepatocellular Carcinoma

Wang, Man; Yu, Fei; Chen, Xinzhe; Li, Peifeng; Wang, Kun

doi:10.1016/j.omtn.2020.05.011

Cited by 35 publications

(29 citation statements)

References 131 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, overexpression of miR-1324 reverses circFoxM1-induced sorafenib resistance and increases MeCP2 expression. This further confirms that circFOXM1 contribute to the regulation of sorafenib sensitivity in HCC cells through the miR-1324/MeCP2 axis (95).…”

Section: Circrnas and Sorafenib Resistance Of Hccsupporting

confidence: 76%

“…However, studies on the role of circRNAs in the sorafenib resistance of HCC are still in the infancy. It has been found 582 differentially expressed circRNAs in HCC cells resistant to sorafenib (HUH7-S), of which 272 were up-regulated and 310 were down-regulated, with a statistically significant difference (0.05) (95). This suggests that circRNAs with different expression levels may exert a crucial role in sorafenib resistance of HCC.…”

Section: Circrnas and Sorafenib Resistance Of Hccmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Non-Coding RNAs in the Sorafenib Resistance of Hepatocellular Carcinoma

Zhu

Shen

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death. Sorafenib is approved by the U.S. Food and Drug Administration to be a first-line chemotherapy agent for patients with advanced HCC. A portion of advanced HCC patients can benefit from the treatment with sorafenib, but many patients ultimately develop sorafenib resistance, leading to a poor prognosis. The molecular mechanisms of sorafenib resistance are sophisticated and indefinite. Notably, non-coding RNAs (ncRNAs), which include long ncRNAs (lncRNAs), microRNAs (miRNAs) and circular RNAs (circRNAs), are critically participated in the occurrence and progression of tumors. Moreover, growing evidence has suggested that ncRNAs are crucial regulators in the development of resistance to sorafenib. Herein, we integrally and systematically summarized the molecular mechanisms and vital role of ncRNAs impact sorafenib resistance of HCC, and ultimately explored the potential clinical administrations of ncRNAs as new prognostic biomarkers and therapeutic targets for HCC.

show abstract

Section: Circrnas and Sorafenib Resistance Of Hccsupporting

confidence: 76%

Section: Circrnas and Sorafenib Resistance Of Hccmentioning

confidence: 99%

The Role of Non-Coding RNAs in the Sorafenib Resistance of Hepatocellular Carcinoma

Zhu

Shen

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

show abstract

“…To date, the conventional chemotherapy treatments in patients with HCC are still not ideal due to the frequently occurring chemoresistance [22,23]. A growing number of studies have showed that the exiting of cancer stem cells and their enrichment during chemotherapy is closely associated with chemotherapy failure and HCC relapse [24][25][26].…”

Section: Discussionmentioning

confidence: 99%

LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3

Shu

Wang

et al. 2021

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Background Hepatocellular carcinoma (HCC) has an extremely poor prognosis due to the development of chemoresistance, coupled with inherently increased stemness properties. Long non-coding RNAs (LncRNAs) are key regulators for tumor cell stemness and chemosensitivity. Currently the relevance between LINC00680 and tumor progression was still largely unknown, with only one study showing its significance in glioblastoma. The study herein was aimed at identifying the role of LINC00680 in the regulation HCC stemness and chemosensitivity. Methods QRT-PCR was used to detect the expression of LINC00680, miR-568 and AKT3 in tissue specimen and cell lines. Gain- or loss-of function assays were applied to access the function of LINC00680 in HCC cells, including cell proliferation and stemness properties. HCC stemness and chemosensitivity were determined by sphere formation, cell viability and colony formation. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were performed to examine the interaction between LINC00680 and miR-568 as well as that between miR-568 and AKT3. A nude mouse xenograft model was established for the in vivo study. Results We found that LINC00680 was remarkably upregulated in HCC tissues. Patients with high level of LINC00680 had poorer prognosis. LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Mechanism study revealed that LINC00680 regulated HCC stemness and chemosensitivity through sponging miR-568, thereby expediting the expression of AKT3, which further activated its downstream signaling molecules, including mTOR, elF4EBP1, and p70S6K. Conclusion LINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3, suggesting that LINC00680 might be a potentially important HCC diagnosis marker and therapeutic target.

show abstract

“…To date, the conventional chemotherapy treatments in patients with HCC are still not ideal due to the frequently occurring chemoresistance (21,22). A growing number of studies have showed that the exiting of cancer stem cells and their enrichment during chemotherapy is closely associated with chemotherapy failure and HCC relapse (23)(24)(25).…”

Section: Discussionmentioning

confidence: 99%

LINC00680 Enhances Hepatocellular Carcinoma Stemness Behavior and Chemoresistance by Sponging miR-568 to Upregulate AKT3

Shu

Wang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Hepatocellular carcinoma (HCC) has an extremely poor prognosis due to the development of chemoresistance, coupled with inherently increased stemness properties. Long non-coding RNAs (LncRNAs) are key regulators for tumor cell stemness and chemosensitivity. Currently the relevance between LINC00680 and tumor progression was still largely unknown, with only one study showing its significance in glioblastoma. The study herein was aimed at identifying the role of LINC00680 in the regulation HCC stemness and chemosensitivity. Methods: QRT-PCR was used to detect the expression of LINC00680, miR-568 and AKT3 in tissue specimen and cell lines. Gain- or loss-of function assays were applied to access the function of LINC00680 in HCC cells, including cell proliferation and stemness properties. HCC stemness and chemosensitivity were determined by sphere formation, cell viability and colony formation. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull down assays were performed to examine the interaction between LINC00680 and miR-568 as well as that between miR-568 and AKT3. A nude mouse xenograft model was established for the in vivo study.Results: We found that LINC00680 was remarkably upregulated both in HCC tissue and cell lines. Patients with high level of LINC00680 had poorer prognosis. LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Mechanism study revealed that LINC00680 regulated HCC stemness and chemosensitivity through sponging miR-568, thereby expediting the expression of AKT3, which further activated its downstream signaling molecules, including mTOR, elF4EBP1, and p70S6K.Conclusion: LINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3, suggesting that LINC00680 might be a potentially important HCC diagnosis marker and therapeutic target.

show abstract

The Underlying Mechanisms of Noncoding RNAs in the Chemoresistance of Hepatocellular Carcinoma

Cited by 35 publications

References 131 publications

The Role of Non-Coding RNAs in the Sorafenib Resistance of Hepatocellular Carcinoma

The Role of Non-Coding RNAs in the Sorafenib Resistance of Hepatocellular Carcinoma

LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3

LINC00680 Enhances Hepatocellular Carcinoma Stemness Behavior and Chemoresistance by Sponging miR-568 to Upregulate AKT3

Contact Info

Product

Resources

About