Catalpol Suppresses Proliferation and Facilitates Apoptosis of OVCAR-3 Ovarian Cancer Cells through Upregulating MicroRNA-200 and Downregulating MMP-2 Expression

Gao, Na; Tian, Jiang; Shang, Yue; Zhao, Danyi; Wu, Tao

doi:10.3390/ijms151119394

Cited by 31 publications

(22 citation statements)

References 22 publications

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“…Recently, the inhibited effect on inflammation and tumor angiogenesis of catalpol in CRC cells was revealed and catalpol was considered as a potential candidate compound for treating CRC (3,10,20). Significant changes in the miRNA expression profiles were observed in cancer cells after catalpol treatment (8)(9)(10)21). Moreover, the present findings indicated that miR-34a played a tumor-suppressive role during progression of human CRC and cholangiocarcinoma (11,12).…”

Section: Discussionsupporting

confidence: 50%

“…Catalpol is one of the main active ingredients of R. glutinosa (Di Huang) which has been revealed to have antitumor effects on various of human cancers (5,(8)(9)(10). Recently, the inhibited effect on inflammation and tumor angiogenesis of catalpol in CRC cells was revealed and catalpol was considered as a potential candidate compound for treating CRC (3,10,20).…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence has demonstrated that miRs are aberrantly expressed in multiple human cancers and stimulate inappropriate cellular programs (7). The antitumor and antiproliferative activities of catalpol are closely associated with aberrant versions of miRs (8)(9)(10), which provides insights on the interaction between catalpol and the expression of miRs. Our previous studies indicated that miR-34a has a tumor-suppressive role in human CRC and cholangiocarcinoma (11,12); thus, we hypothesized that there may be a correlation between catalpol and miR-34a in the progression of CRC.…”

Section: Introductionmentioning

confidence: 99%

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Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

2020

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Colorectal cancer (CRC) is one of the most common digestive tract tumors worldwide. Catalpol exerts inhibitory effects on the progression of several cancer types by regulating microRNAs (miRs). However, the precise role and carcinostatic mechanism of catalpol on CRC cells are poorly understood which limits the application of catalpol treatment. In the present study, miR-34a and sirtuin 1 (SIRT1) expression levels were detected in CRC tissues and CRC cell lines by RT-qPCR. Computational software analysis, luciferase assays and western blotting were used to demonstrate the downstream target of miR-34a in CRC cells. Effects of catalpol on cell viability, apoptosis, autophagic flux and the miR-34a/SIRT1 axis in the CRC cells were assessed by CCK-8 assay, flow cytometry, electron microscopy and western blotting, respectively. Whether the miR-34a/SIRT1 axis participated in catalpol-mediated autophagy and apoptosis was investigated. The effects of catalpol on the miR-34a/SIRT1 axis and malignant behavior were evaluated in a rat model of azoxymethane (AOM)-induced CRC. It was revealed that miR-34a expression levels were significantly decreased while SIRT1 was overexpressed in most of the CRC tissues and all the CRC cell lines. Clinically, a low level of miR-34a was correlated with poor clinicopathological characteristics in CRC patients. Catalpol reduced cell viability, suppressed autophagy, promoted apoptosis, and regulated the expression of SIRT1 by inducing miR-34a in vitro and in vivo. The autophagy-inhibiting effect of catalpol may be a mechanism to promote apoptosis of CRC cells. miR-34a mimic transfection resulted in autophagy-suppressive activity similar to that of catalpol, while the miR-34a inhibitor attenuated the antiautophagic effects of catalpol. In conclusion, miR-34a is involved in regulating catalpol-mediated autophagy and malignant behavior by directly inhibiting SIRT1 in CRC.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

2020

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“…A previous study demonstrated that microRNA-200 exhibits a regulatory role in the proliferation of gastric cancer MGC-803 cells and that overexpression of microRNA-200 may inhibit the proliferation of gastric cancer MGC-803 cells (24)(25)(26)(27). Gao et al (28) reported that catalpol suppresses proliferation and facilitates apoptosis in OVCAR-3 ovarian cancer cells through activation of microRNA-200 and downregulating matrix metalloproteinase-2 expression. In the The PI3K/Akt signal transduction pathway serves an important role in cell proliferation, in which Akt is a downstream target protein of PI3K, and continuous activation of the pathway is associated with tumor development (29).…”

Section: Discussionmentioning

confidence: 99%

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway

et al. 2017

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Abstract.Catalpol is an effective active ingredient that functions as a diuretic and laxative, and exhibits blood sugar-lowering, liver protective, anti-aging and anticancer effects. In traditional Chinese medicine, catalpol is believed to be Yin nourishing. The anticancer effect of catalpol on human HCT116 colorectal cancer cells were investigated and the mechanism of action was evaluated. Cellular viability was detected using an MTT assay. Caspase-3 and caspase-9 activity, cellular apoptosis and nucleic morphology were analyzed using caspase-3 and caspase-9 activity assay kits, flow cytometric assays and DAPI staining assay, respectively. Western blot analysis was used to measure the protein expressions of phosphatidylinositol 3-kinase (PI3K), phosphorylated-protein kinase B (p-Akt) and Akt. Expression of microRNA-200 was detected using the reverse transcription-quantitative polymerase chain reaction. HCT116 cells were incubated with PI3K inhibitors in order to analyze the effect of catalpol on cell proliferation. Catalpol was able to inhibit HCT116 cell proliferation. Furthermore, catalpol induced apoptosis in HCT116 cells, which depended on the increased activities of caspase-3 and -9. In addition, catalpol reduced the expression of PI3K, p-Akt and Akt in HCT116 cells. However, downregulation of PI3K/Akt decreased the viability of HCT116 cells following treatment with catalpol and enhanced microRNA-200 expression. Catalpol promoted cellular apoptosis in human HCT116 colorectal cancer cells through upregulation of microRNA-200 expression, which depended on a downregulation of the phosphatase and tensin homolog/PI3K-Akt signaling pathway.

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“…MicroRNAs (miRs) are short, endogenous, non-coding RNAs that modulate several physiological and pathophysiologic processes including proliferation, differentiation, and apoptosis-via post-transcriptional regulation of target gene expression [1][2][3]. During the past ten years, most miRs have been proved to contribute to tumor suppression by induction of cell-cycle arrest and apoptosis [4].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of microRNA-99a against focal cerebral ischemia–reperfusion injury in mice

Tao

Zhao

Wang

et al. 2015

Journal of the Neurological Sciences

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Catalpol Suppresses Proliferation and Facilitates Apoptosis of OVCAR-3 Ovarian Cancer Cells through Upregulating MicroRNA-200 and Downregulating MMP-2 Expression

Cited by 31 publications

References 22 publications

Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway

Neuroprotective effect of microRNA-99a against focal cerebral ischemia–reperfusion injury in mice

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