LncRNA DARS-AS1 aggravates the growth and metastasis of hepatocellular carcinoma via regulating the miR-3200-5p-Cytoskeleton associated protein 2 (CKAP2) axis

Feng, Yanqing; Wei, Gang; Zhang, Linfei; Zhou, Huadong; Wang, Wei; Guo, Peng; Cheng, Caitao; Ji, Lei; Cai, Qing; Feng, Yong; Tu, Hanjun

doi:10.1080/21655979.2021.1982272

Cited by 26 publications

(14 citation statements)

References 47 publications

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“…The changes in miRNAs observed by high-throughput sequencing suggest that miR-3200-5p is the most critical. This regulatory mechanism of miR-3200-5p is competitively inhibited by DARS-AS1 and targets the cytoskeleton-associated protein 2 (CKAP2) to aggravate the growth and invasion of hepatocellular carcinoma [ 38 ]. In addition, miR-3200-5p acts as a sponge for circMTO1 [ 39 ] and LINC00324 [ 40 ] to attenuate tumorigenesis of gastric carcinoma and promotes osteosarcoma cell migration and invasion by negatively regulating BRMS1 expression [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of HULC Induces Ferroptosis in Hepatocellular Carcinoma via Targeting of the miR-3200-5p/ATF4 Axis

Guan

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Hepatocellular carcinoma is a malignant tumor that poses a serious threat to human health. Ferroptosis, which represents an identified type of regulated iron-dependent cell death, may play an important role in hepatocellular carcinoma. However, it is unclear as to whether ferroptosis is involved with the mechanisms of lncRNA HULC in liver cancer cells. Here, we show that knockdown of HULC increases ferroptosis and oxidative stress in liver cancer cells. We also found changes in some related miRNAs in cells treated with HULC siRNA. Differential miRNA expression levels were determined with the use of high-throughput sequencing and prediction target genes identified using bioinformatics analysis. HULC was found to function as a ceRNA of miR-3200-5p, and miR-3200-5p regulates ferroptosis by targeting ATF4, resulting in the inhibition of proliferation and metastasis within HCC cells. In summary, these findings illuminate some of the molecular mechanisms through which downregulation of HULC induces liver cancer cell ferroptosis by targeting the miR-3200-5p/ATF4 axis to modulate the development of hepatocellular carcinoma.

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Section: Discussionmentioning

confidence: 99%

Downregulation of HULC Induces Ferroptosis in Hepatocellular Carcinoma via Targeting of the miR-3200-5p/ATF4 Axis

Guan

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…After treatment with 0.25% trypsin Ethylene Diamine Tetraacetie Acid (EDTA) (Thermo Fisher Hyclone, Utah, USA), the cells were sub-cultured three times a week. Cells in the logarithmic growth phase were adopted for the following test [ 18 ]. β-Patchoulene (Molecular Formula:C 15 H 24 ) was isolated from the essential oil of Pogostemon cablin as previously described [ 19 ].…”

Section: Methodsmentioning

confidence: 99%

β-Patchoulene represses hypoxia-induced proliferation and epithelial-mesenchymal transition of liver cancer cells

Wang

Feng

et al. 2022

Bioengineered

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Hepatocellular carcinoma (HCC) is a malignant tumor originating from liver epithelial cells with a high clinical mortality rate. β-Patchoulene (β-PAE) is a compound extracted from patchouli, which has analgesic, anti-inflammatory and antioxidant effects. This research aims to probe the impacts of β-PAE on hypoxia-induced HCC cell proliferation and epithelial-mesenchymal transition (EMT). Firstly, hypoxic injury models were constructed in HCC Huh-7 and MHCC97 cells, and the hypoxic injury cell models were then treated with different concentrations of β-PAE. The cell viability, proliferation, migration, invasion and apoptosis were checked by the cell counting kit-8 (CCK-8) assay, colony formation assay, Transwell assay, flow cytometry and terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay. The expression of Survivin protein, EMT markers and the NF-κB/HIF-1α pathway was gauged by Western blot (WB) or cellular immunofluorescence or reverse transcription-polymerase chain reaction (RT-PCR). The in-vivo experiment was conducted to confirm the anti-tumor role of β-PAE. As a result, β-PAE abated hypoxia-induced HCC cell growth, proliferation, migration, invasion and EMT and facilitated apoptosis in vitro and in vivo dose-dependently. Further mechanism studies displayed that β-PAE inactivated the NF-κB/HIF-1α pathway, and HIF-1α activation significantly reversed the β-PAE-mediated tumor inhibition. β-PAE repressed the proliferation and EMT of hypoxia-induced HCC cells by choking the NF-κB/HIF-1α pathway, suggesting that β-PAE was a potential drug for HCC treatment.

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“…The conducted animal study was permitted and strictly adheres to the approval of the Care and Use of Laboratory Animals. The method was followed the previous study [ 32 ]. HCC cells were prepared and injected into BALB/c nude mice for the tumor model construction.…”

Section: Methodsmentioning

confidence: 99%

LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis

Zhou

Zou

et al. 2021

Bioengineered

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Recent years have seen much effect in revealing the pathological association between lncRNA and HCC. Herein, we identified lncRNA DHRS4-AS1 as a potential tumor suppressor in HCC. Firstly, it was discovered that DHRS4-AS1 was significantly down-regulated in HCC tissues compared to normal tissues based on the database TCGA. It was also detected in a lower-than-usual expression quantity in HCC tissues we collected and HCC cell lines. Kaplan-Meier survival analysis revealed that high expression of DHRS4-AS1 contributed to higher overall survival rate of HCC patients.DHRS4-AS1 expression was significantly correlated to tumor size ( P = 0.02) and TNM stage ( P = 0.045). CCK-8, BrdU and colony-forming assays collectively demonstrated that overexpression of DHRS4-AS1 significantly restrained HCC cell proliferation. In vivo xenograft animal experiment showed that DHRS4-AS1 could efficiently preclude the tumor growth of HCC. Further investigation performed using flow cytometry and western blot showed that DHRS4-AS1 exerted its effects by accelerating cell apoptosis and capturing cell cycle in G0/G1 phase. Our study subsequently lucubrated that miR-522-3p was a negative target of DHRS4-AS1. Increased expression level of miR-522-3p was examined in HCC tissues and cell lines. Similarly, miR-522-3p mimics could reverse the inhibitory effect on HCC brought by DHRS4-AS1. SOCS5 was then discovered as a down-stream target of miR-522-3p, which suggested that SOCS5 participated in DHRS4-AS1/miR-522-3p axis to collectively mediate the development of HCC. Our study provides lncRNA DHRS4-AS1/miR-522-3p/SOCS5 axis as a novel target for HCC therapeutic strategy with potentiality.

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LncRNA DARS-AS1 aggravates the growth and metastasis of hepatocellular carcinoma via regulating the miR-3200-5p-Cytoskeleton associated protein 2 (CKAP2) axis

Abstract: Tu (2021): LncRNA DARS-AS1 aggravates the growth and metastasis of hepatocellular carcinoma via regulating the miR-3200-5p-Cytoskeleton associated protein 2 (CKAP2) axis, Bioengineered,

Cited by 26 publications

References 47 publications

Downregulation of HULC Induces Ferroptosis in Hepatocellular Carcinoma via Targeting of the miR-3200-5p/ATF4 Axis

Downregulation of HULC Induces Ferroptosis in Hepatocellular Carcinoma via Targeting of the miR-3200-5p/ATF4 Axis

β-Patchoulene represses hypoxia-induced proliferation and epithelial-mesenchymal transition of liver cancer cells

LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis

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