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Induction of human chronic myeloid leukemia K562 cell apoptosis by virosecurinine and its molecular mechanism.

Zhang G, Li M, Han S, Chen D, Wang Y, Ye W, Ji Z - Mol Med Rep (2014)

Bottom Line: The present study aimed to investigate the antitumor effects of virosecurinine by inducing the apoptosis of leukemic K562 cells and to examine the underlying mechanisms.The generation depression effects of K562 cells cultured in vitro were detected using CCK‑8 technology, which revealed a dose and time‑dependent association.Virosecurinine inhibited the growth and proliferation of the K562 cell lines and induced apoptosis in K562 cells by affecting the expression of mTOR, SHIP2, BCR/ABL and PTEN.

View Article: PubMed Central - PubMed

Affiliation: Department of Oncology, Wannan Medical College, Wuhu, Anhui 241001, P.R. China.

ABSTRACT
Virosecurinine is a major alkaloid of the plant Securinega suffruticosa and has been found to be a potent agent in inducing the differentiation of cancer cells. The present study aimed to investigate the antitumor effects of virosecurinine by inducing the apoptosis of leukemic K562 cells and to examine the underlying mechanisms. K562 cells were treated with different concentrations of virosecurinine (6.25, 12.5, 25, 50, 100 and 200 µmol/l) for 24, 48 and 72 h. The cell counting kit (CCK)‑8 method was used to detect the antitumor effect of K562 cells in vitro. Flow cytometry was used to observe the apoptotic ratio and analyze the cell cycle following treatment with virosecurinine in K562 cells. Light and electron microscopy was used to identify morphological alterations in the virosecurinine‑treated K562 cells. The mRNA levels of mammalian target of rapamycin (mTOR), SH2 domain‑containing inositol‑5'‑phosphatase 2 (SHIP2), phosphatase and tensin homologue (PTEN) and breakpoint cluster region (BCR)/Abelson (ABL) were detected pre and post‑virosecurinine treatment using reverse transcription quantitative polymerase chain reaction (RT‑qPCR). The generation depression effects of K562 cells cultured in vitro were detected using CCK‑8 technology, which revealed a dose and time‑dependent association. The IC50 was 32.984 µmol/l at 48 h. Flow cytometric analysis indicated that treatment with virosecurinine at concentrations of 6.25, 25 and 50 µmol/l increased the apoptotic rate of the K562 cells and caused G1/S phase arrest. RT‑qPCR indicated that virosecurinine upregulated the gene expression of PTEN and downregulated the expression of mTOR, SHIP‑2 and BCR/ABL in K562 cells. Virosecurinine inhibited the growth and proliferation of the K562 cell lines and induced apoptosis in K562 cells by affecting the expression of mTOR, SHIP2, BCR/ABL and PTEN.

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Reverse transcription quantitative polymerase chain reaction analysis of genes in K562 cells treated with virosecurinine at 6.25, 25 and 50 μmol/l for 48 h. mTOR, mammalian target of rapamycin; SHIP2, SH2 domain-containing inositol-5′-phosphatase 2; PTEN, phosphatase and tensin homologue; BCR, breakpoint cluster region; ABL, Abelson.
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f8-mmr-10-05-2365: Reverse transcription quantitative polymerase chain reaction analysis of genes in K562 cells treated with virosecurinine at 6.25, 25 and 50 μmol/l for 48 h. mTOR, mammalian target of rapamycin; SHIP2, SH2 domain-containing inositol-5′-phosphatase 2; PTEN, phosphatase and tensin homologue; BCR, breakpoint cluster region; ABL, Abelson.

Mentions: In order to further understand the molecular mechanism underlying virosecurinine-induced apoptosis, the mRNA levels of mTOR, PTEN, BCR/ABL and SHIP2 mRNA were measured in virosecurinine-deprived and control K562 cells using RT-qPCR analysis. The results indicated that virosecurinine effectively downregulated the expression level of mTOR, SHIP2 and BCR/ABL and upregulated the expression of PTEN (P<0.05; Fig. 8).


Induction of human chronic myeloid leukemia K562 cell apoptosis by virosecurinine and its molecular mechanism.

Zhang G, Li M, Han S, Chen D, Wang Y, Ye W, Ji Z - Mol Med Rep (2014)

Reverse transcription quantitative polymerase chain reaction analysis of genes in K562 cells treated with virosecurinine at 6.25, 25 and 50 μmol/l for 48 h. mTOR, mammalian target of rapamycin; SHIP2, SH2 domain-containing inositol-5′-phosphatase 2; PTEN, phosphatase and tensin homologue; BCR, breakpoint cluster region; ABL, Abelson.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4214351&req=5

f8-mmr-10-05-2365: Reverse transcription quantitative polymerase chain reaction analysis of genes in K562 cells treated with virosecurinine at 6.25, 25 and 50 μmol/l for 48 h. mTOR, mammalian target of rapamycin; SHIP2, SH2 domain-containing inositol-5′-phosphatase 2; PTEN, phosphatase and tensin homologue; BCR, breakpoint cluster region; ABL, Abelson.
Mentions: In order to further understand the molecular mechanism underlying virosecurinine-induced apoptosis, the mRNA levels of mTOR, PTEN, BCR/ABL and SHIP2 mRNA were measured in virosecurinine-deprived and control K562 cells using RT-qPCR analysis. The results indicated that virosecurinine effectively downregulated the expression level of mTOR, SHIP2 and BCR/ABL and upregulated the expression of PTEN (P<0.05; Fig. 8).

Bottom Line: The present study aimed to investigate the antitumor effects of virosecurinine by inducing the apoptosis of leukemic K562 cells and to examine the underlying mechanisms.The generation depression effects of K562 cells cultured in vitro were detected using CCK‑8 technology, which revealed a dose and time‑dependent association.Virosecurinine inhibited the growth and proliferation of the K562 cell lines and induced apoptosis in K562 cells by affecting the expression of mTOR, SHIP2, BCR/ABL and PTEN.

View Article: PubMed Central - PubMed

Affiliation: Department of Oncology, Wannan Medical College, Wuhu, Anhui 241001, P.R. China.

ABSTRACT
Virosecurinine is a major alkaloid of the plant Securinega suffruticosa and has been found to be a potent agent in inducing the differentiation of cancer cells. The present study aimed to investigate the antitumor effects of virosecurinine by inducing the apoptosis of leukemic K562 cells and to examine the underlying mechanisms. K562 cells were treated with different concentrations of virosecurinine (6.25, 12.5, 25, 50, 100 and 200 µmol/l) for 24, 48 and 72 h. The cell counting kit (CCK)‑8 method was used to detect the antitumor effect of K562 cells in vitro. Flow cytometry was used to observe the apoptotic ratio and analyze the cell cycle following treatment with virosecurinine in K562 cells. Light and electron microscopy was used to identify morphological alterations in the virosecurinine‑treated K562 cells. The mRNA levels of mammalian target of rapamycin (mTOR), SH2 domain‑containing inositol‑5'‑phosphatase 2 (SHIP2), phosphatase and tensin homologue (PTEN) and breakpoint cluster region (BCR)/Abelson (ABL) were detected pre and post‑virosecurinine treatment using reverse transcription quantitative polymerase chain reaction (RT‑qPCR). The generation depression effects of K562 cells cultured in vitro were detected using CCK‑8 technology, which revealed a dose and time‑dependent association. The IC50 was 32.984 µmol/l at 48 h. Flow cytometric analysis indicated that treatment with virosecurinine at concentrations of 6.25, 25 and 50 µmol/l increased the apoptotic rate of the K562 cells and caused G1/S phase arrest. RT‑qPCR indicated that virosecurinine upregulated the gene expression of PTEN and downregulated the expression of mTOR, SHIP‑2 and BCR/ABL in K562 cells. Virosecurinine inhibited the growth and proliferation of the K562 cell lines and induced apoptosis in K562 cells by affecting the expression of mTOR, SHIP2, BCR/ABL and PTEN.

Show MeSH
Related in: MedlinePlus