Tanshinol inhibits the growth, migration and invasion of hepatocellular carcinoma cells via regulating the PI3K-AKT signaling pathway

Zhu, Pingting; Liu, Zhaoguo; Zhou, Jiaojiao; Chen, Yuanyuan

doi:10.2147/ott.s185997

Cited by 24 publications

(15 citation statements)

References 43 publications

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“…Taken together, these results demonstrated that MAFG-AS1 may promote HCC progression through inhibition of miR-6852. The effect of MAFG-AS1 on expression of members of the STAT3, Wnt/β-catenin and PI3K/AKT signaling pathways were determined, which are related to proliferation, migration and invasion of HCC (19). Western blotting showed that MAFG-AS1 silencing only suppressed the activation of the PI3K/AKT signaling pathway (Fig.…”

Section: Resultsmentioning

confidence: 99%

Long noncoding RNA MAFG‑AS1 promotes proliferation, migration and invasion of hepatocellular carcinoma cells through downregulation of miR‑6852

et al. 2019

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Long noncoding RNAs (lncRNAs) have been shown to participate in the development and progression of a number of different types of cancer, including hepatocellular carcinoma (HCC). A recent report has indicated that lncRNA MAFG-antisense 1 (AS1) promotes colorectal cancer. However, the role of MAFG-AS1 in other types of cancer remains unclear. The aim of the present study was to examine the effect of lncRNA MAFG-AS1 in HCC. Based on The Cancer Genome Atlas database and reverse transcription-quantitative PCR results, it was determined that lncRNA MAFG-AS1 expression was increased in HCC tissues and cell lines. Following knockdown of lncRNA MAFG-AS1, a Cell Counting Kit-8 assay and Transwell assay demonstrated that the proliferation, migration and invasion of HCC cell lines were significantly inhibited. It was additionally demonstrated that there was a negative regulatory association between lncRNA MAFG-AS1 and miR-6852. Inhibition of miR-6852 increased proliferation, migration and invasion of HCC cell lines. LncRNA MAFG-AS1 promoted HCC development by dampening miR-6852 function and may thus be a novel target for treating patients with HCC.

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Section: Resultsmentioning

confidence: 99%

Long noncoding RNA MAFG‑AS1 promotes proliferation, migration and invasion of hepatocellular carcinoma cells through downregulation of miR‑6852

et al. 2019

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“…Regarding the PI3K-Akt signaling pathway, numerous studies have also reported its crucial role in the process of HCC. The PI3K-Akt signaling pathway has been widely reported to act as a key factor related to cell proliferation, invasion, metastasis, and apoptosis as well as the cell cycle [52][53][54][55][56]. Given that, we speculated that the molecular mechanism of CELSR3 in promoting cell proliferation, invasion, and migration, as well as inhibiting apoptosis may be closely associated with the cell cycle, DNA replication, and the PI3K-Akt signaling pathway through interacting with its co-expressed genes.…”

Section: Discussionmentioning

confidence: 93%

Effect of CELSR3 on the Cell Cycle and Apoptosis of Hepatocellular Carcinoma Cells

Xie

Dang

et al. 2020

J. Cancer

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Cadherin EGF LAG seven-pass G-type receptor 3 (CELSR3) has been reported in cancers but its role and potential molecular mechanism in hepatocellular carcinoma (HCC) is unclear. Therefore, we aimed to investigate the clinical value and molecular mechanism of CELSR3 in HCC using an in vitro experiment, a meta-analysis and bioinformatics. The in vitro experiment determined the promoting effect of CELSR3 in the proliferation, invasion, and migration of HCC cells. CELSR3 knockout causes S-phage arrest in HCC cells. CELSR3 can also inhibit the apoptosis of HCC cells. The expression of the CELSR3 gene and protein was significantly elevated in HCC. Elevated CELSR3 was correlated to the bigger tumor size, higher pathological stage, and the worse overall survival of HCC. Methylation analysis revealed that the hypomethylation of CELSR3 regulated by DNMT1, DNMT3A, and DNMT3B may be the underlying mechanism of upregulated CELSR3. Biological enrichment analysis uncovered that the cell cycle, DNA replication, and PI3K-Akt signaling pathways were important pathways regulated by CELSR3 and its co-expressed genes in HCC. Taken together, upregulated CELSR3 is an important regulator in the progression and prognosis of HCC. The hypomethylation of CELSR3 and its regulation in the cell cycle may be the potential molecular mechanism in HCC.

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“…no. IT4738; G-Biosciences) in the culture media according to the manufacturer's instructions and as described previously (31,32).…”

Section: Methodsmentioning

confidence: 99%

Effects of histone H4 hyperacetylation on inhibiting MMP2 and MMP9 in human amniotic epithelial cells and in premature rupture of fetal membranes

Song¹,

Yang²,

Hu³

et al. 2021

Exp Ther Med

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Histone modification is closely associated with several diseases. The aim of the current study was to investigate the associations among histone acetylation, matrix metalloproteinases (MMPs) and premature rupture of membranes (PROM) during pregnancy. A total of 180 puerperants were divided into three groups: i) Preterm-PROM (PPROM), ii) term-PROM (TPROM) and iii) full-term labor (FTL). Enzyme-linked immunosorbent assay (ELISA) kits and western blotting were used to determine the protein concentrations of MMP2, MMP9, histone deacetylase (HDAC)1, HDAC2 and HDAC6, and the protein levels of histone H4 lysine (H4K)5 and H4K8 acetylation, respectively, in three types of fetal membranes. Additionally, human amniotic epithelial cells were used to determine the effects of the HDAC inhibitors droxinostat and chidamide on cell viability, histone acetylation and the levels of MMP2, MMP9, HDAC1, HDAC2 and HDAC6 in vitro, using the Cell Counting Kit-8 assay, western blotting and ELISA, respectively. Furthermore, the effects of droxinostat and chidamide on the invasion and migration abilities of human amniotic epithelial cells were investigated using transwell assays. In fetal membranes, the activities of MMP2 and MMP9 increased in PPROM, but decreased in TPROM. Further, the expression of HDAC1 was decreased and histone hyperacetylation was increased in both PPROM and TRPOM. In vitro experiments revealed that 5 µM droxinostat and 0.5 µM chidamide selectively decreased the level of HDAC and induced acetylation of H4K5 and H4K8. Additionally, the aforementioned HDAC inhibitors reduced human amniotic epithelial cell viability, invasion and migration, and decreased the expression levels of MMP2 and MMP9. The current study revealed a high expression level of MMP2 and MMP9 in PPROM compared with TPROM and FL tissue, which was in accordance with previously published studies. Furthermore, the in vitro tests performed in the current study revealed the effect of histone H4 hyperacetylation on inhibiting MMP2 and MMP9 levels in vitro was similar to that observed in TPROM. The results obtained in the current study may be used as a theoretical guide for clinical treatment of premature rupture of membranes.

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Tanshinol inhibits the growth, migration and invasion of hepatocellular carcinoma cells via regulating the PI3K-AKT signaling pathway

Cited by 24 publications

References 43 publications

Long noncoding RNA MAFG‑AS1 promotes proliferation, migration and invasion of hepatocellular carcinoma cells through downregulation of miR‑6852

Long noncoding RNA MAFG‑AS1 promotes proliferation, migration and invasion of hepatocellular carcinoma cells through downregulation of miR‑6852

Effect of CELSR3 on the Cell Cycle and Apoptosis of Hepatocellular Carcinoma Cells

Effects of histone H4 hyperacetylation on inhibiting MMP2 and MMP9 in human amniotic epithelial cells and in premature rupture of fetal membranes

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