LncRNA NEAT1 modulates sorafenib resistance in hepatocellular carcinoma through regulating the miR-149-5p/AKT1 axis

Niu, Yuexiang; Tang, Gongen; Wu, Xiuli; Wu, Chaoyu

doi:10.4103/sjg.sjg_4_20

Cited by 25 publications

(12 citation statements)

References 28 publications

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“…A large number of studies have pointed out that the expression of lncRNA is related to the resistance of anti-tumor drugs (19)(20)(21). We sought to investigate the impact of LINC01667 modulation in HCC-derived cell lines upon Sorafenib and Regorafenib exposure in vitro.…”

Section: Linc01667 May Increase the Chemical Sensitivity Of Sorafenib And Regorafenib But No Synergistic Effectmentioning

confidence: 99%

Upregulated LINC01667 Expression Is Correlated With Poor Prognosis in Hepatocellular Carcinoma

Zhang

Liu

et al. 2021

Front. Oncol.

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The development of hepatocellular carcinoma (HCC) is a complex pathological process. Long intergenic non–protein-coding RNA 1667 (LINC01667, also known as MGC38584) plays an oncogenic role in several human cancers; however, its functional role in HCC tumorigenesis remains unknown. Here, we first evaluated the gene expression levels of LINC01667 in HCC using data from The Cancer Genome Atlas and Gene Expression Profiling Interactive Analysis (GEPIA) databases. We then elucidated the association between LINC01667 gene expression levels and the survival rates of patients with HCC. We detected the effect of LINC01667 on the malignant phenotypes (cell proliferation, migration, invasion and apoptosis etc.) and the MAPK and PI3K/AKT/mTOR signaling pathways of HepG2, SMMC-7721 and HUH7 cells. We also analyzed the sensitivity of HepG2, SMMC-7721 and HUH7 with different expression levels of LINC01667 to anti-HCC drugs in vitro. Based on data from the aforementioned databases and our experiments in vitro, we found that LINC01667 was overexpressed in HCC, and that patients with high LINC01667 levels had a remarkably poor overall survival rate. In addition, inhibition of LINC01667 expression suppressed the proliferation, migration and invasion of HepG2 and SMMC-7721 cells and promoted their apoptosis in vitro. In contrast, overexpression of LINC01667 promoted the proliferation, migration and invasion of HUH7 cells and suppressed their apoptosis in vitro. ChIRP-seq (chromatin isolation by RNA purification) showed that LINC01667 bound to MEG3, and downregulated the expression of MEG3. In addition, western blotting showed that LINC01667 could activate the NF-κB pathway to promote cancer progression. In conclusion, we report that LINC01667 is an important oncogene in HCC and may be used as a potential diagnostic and prognostic biomarker of HCC.

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Section: Linc01667 May Increase the Chemical Sensitivity Of Sorafenib And Regorafenib But No Synergistic Effectmentioning

confidence: 99%

Upregulated LINC01667 Expression Is Correlated With Poor Prognosis in Hepatocellular Carcinoma

Zhang

Liu

et al. 2021

Front. Oncol.

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“…e hub targets identified from the analysis of the FDY003-associated PPI network modulate crucial LC pathological mechanisms, and this targeting may result in effective therapeutic effects against LC. AKT1 is an important regulator of the tumorigenic processes, migration, Evidence-Based Complementary and Alternative Medicine spreading, therapeutic sensitivity, resistance, survival, and proliferation of LC cells, and is a promising theragnostic target [64][65][66][67]. AR expression and activity influence angiogenesis, stemness, invasion, angiogenesis, epithelialmesenchymal transition (EMT), migration, and oncogenesis of LC cells, and it is a prognostic determinant and responsive marker for anticancer therapies [68][69][70][71][72][73].…”

Section: Discussionmentioning

confidence: 99%

Investigation of Anti-Liver Cancer Activity of the Herbal Drug FDY003 Using Network Pharmacology

Lee

Park³

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Globally, liver cancer (LC) is the sixth-most frequently occurring and the second-most fatal malignancy, responsible for 0.83 million deaths annually. Although the application of herbal drugs in cancer therapies has increased, their anti-LC activity and relevant mechanisms have not been fully studied from a systems perspective. To address these issues, we conducted a system-perspective network pharmacological investigation into the activity and mechanisms underlying the action of the herbal drug. FDY003 reduced the viability of human LC treatment. FDY003 reduced the viability of human LC cells and elevated their chemosensitivity. There were a total of 16 potential bioactive chemical components in FDY003 and they had 91 corresponding targets responsible for the pathological processes in LC. These FDY003 targets were functionally involved in regulating the survival, proliferation, apoptosis, and cell cycle of LC cells. Additionally, we found that FDY003 may target key signaling cascades connected to diverse LC pathological mechanisms, namely, PI3K-Akt, focal adhesion, IL-17, FoxO, MAPK, and TNF pathways. Overall, this study contributed to integrative mechanistic insights into the anti-LC potential of FDY003.

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“…LncNEAT1, which also plays a pro-oncogenic role, is significantly increased in HCC cells. It inhibits the efficacy of sorafenib by targeting miR-149-5p and regulating the miR-149-5p/AKT1 axis (47). Furthermore, NEAT1 inhibits the sensitivity of HCC cells to sorafenib via modulating miR-335/c-Met (58).…”

Section: Acting On Akt Activationmentioning

confidence: 99%

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

Zhu

Shen

et al. 2021

Front. Oncol.

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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.

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LncRNA NEAT1 modulates sorafenib resistance in hepatocellular carcinoma through regulating the miR-149-5p/AKT1 axis

Cited by 25 publications

References 28 publications

Upregulated LINC01667 Expression Is Correlated With Poor Prognosis in Hepatocellular Carcinoma

Upregulated LINC01667 Expression Is Correlated With Poor Prognosis in Hepatocellular Carcinoma

Investigation of Anti-Liver Cancer Activity of the Herbal Drug FDY003 Using Network Pharmacology

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

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