Dataset Information

Piceatannol suppresses proliferation and induces apoptosis by regulation of the microRNA?21/phosphatase and tensin homolog/protein kinase B signaling pathway in osteosarcoma cells.

ABSTRACT: Piceatannol (Pice), a natural analog of resveratrol, has been identified as an anticancer agent in various cancers by modulating the expression of microRNAs (miRNAs/miRs). However, the molecular mechanisms underlying the anticancer effects of Pice in osteosarcoma (OS) cells remain unclear. Thus, we hypothesized that Pice exerts anticancer effects on OS cells via the regulation of miRNA expression. Herein, we performed a MTT assay and flow cytometric analysis to determine cell viability and apoptosis in OS cells treated with Pice, respectively. Our results showed that Pice inhibits proliferation in a dose?dependent manner induces the apoptosis of OS cells. More importantly, miRNA microarray analysis identified that Pice alters miRNA expression profiles in human OS cells after treatment with Pice, and miR?21 was the most significantly downregulated. In addition, the therapeutic effects of Pice on OS cells were weakened by restoration of miR?21. In addition, we further verified that phosphatase and tensin homolog (PTEN), a tumor suppressor gene, is the functional target of miR?21 and Pice blocks the PTEN/AKT signaling pathway through inhibiting miR?21 expression in OS cells. Our findings suggested that Pice may exert anticancer effects on OS cells via mediating the miR?21/PTEN/AKT signaling pathway and could be considered to be a potential anticancer agent for treating OS.

SUBMITTER: Zheng M

PROVIDER: S-EPMC7533446 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Piceatannol suppresses proliferation and induces apoptosis by regulation of the microRNA‑21/phosphatase and tensin homolog/protein kinase B signaling pathway in osteosarcoma cells.

Zheng Mingyue M Wu Yaochi Y

Molecular medicine reports 20200902 5

Piceatannol (Pice), a natural analog of resveratrol, has been identified as an anticancer agent in various cancers by modulating the expression of microRNAs (miRNAs/miRs). However, the molecular mechanisms underlying the anticancer effects of Pice in osteosarcoma (OS) cells remain unclear. Thus, we hypothesized that Pice exerts anticancer effects on OS cells via the regulation of miRNA expression. Herein, we performed a MTT assay and flow cytometric analysis to determine cell viability and apopt ...[more]

PMID: 32901863

Similar Datasets

Project description:Honokiol (HNK) is a small biphenolic compound, which exerts antineoplastic effects in various types of cancer. However, the mechanism underlying the antitumor effects of HNK in osteosarcoma (OS) cells is not yet fully understood. Emerging evidence has indicated that microRNAs (miRNAs/miRs) serve key roles in numerous pathological processes, including cancer. It has previously been reported that Chinese medicinal herbs harbor anticancer properties via modulating miRNA expression. Therefore, the present study aimed to determine whether HNK could suppress OS cell growth by regulating miRNA expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometric analysis were used to evaluate the cell proliferation and apoptosis in human OS cells after treatment with HNK, respectively. The results demonstrated that HNK inhibits proliferation and induces apoptosis of human OS cells in a dose?dependent manner. Furthermore, HNK?induced apoptosis was characterized by upregulation of proapoptotic proteins, including cleaved?caspase?3, cleaved?poly (ADP?ribose) polymerase and B?cell lymphoma 2 (Bcl?2)?associated X protein, and downregulation of the anti?apoptotic protein Bcl?2. Reverse transcription?quantitative polymerase chain reaction (RT?qPCR) verified that HNK was able to induce aberrant expression of miRNAs in human OS cells, and miR?21 was one of the miRNAs that was most significantly downregulated. To further investigate miR?21 function, the present study validated that HNK reduces miR?21 levels in a dose?dependent manner. In addition, restoration of miR?21 expression abrogated the suppressive effects of HNK on OS cells. Luciferase assay and western blot analysis identified that miR?21 inhibits the expression of phosphatase and tensin homolog (PTEN) by directly targeting its 3'-UTR. Notably, HNK was able to suppress the phosphoinositide 3?kinase (PI3K)/protein kinase B (AKT) signaling pathway; however, it was reactivated by miR?21 overexpression. Taken together, these data indicated that HNK may inhibit proliferation and induce apoptosis of human OS cells by modulating the miR?21/PTEN/PI3K/AKT signaling pathway. Therefore, miR?21 may be considered a potential therapeutic target for the treatment of osteosarcoma with HNK.

Dataset Information

Piceatannol suppresses proliferation and induces apoptosis by regulation of the microRNA?21/phosphatase and tensin homolog/protein kinase B signaling pathway in osteosarcoma cells.

Publications

Piceatannol suppresses proliferation and induces apoptosis by regulation of the microRNA‑21/phosphatase and tensin homolog/protein kinase B signaling pathway in osteosarcoma cells.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets