Effect of TIEG1 on apoptosis and expression of Bcl-2/Bax and Pten in leukemic cell lines

Abstract

ABSTRACT.We examined the effect of transforming growth factor-b inducible early gene-1 (TIEG1) on the apoptosis of leukemic cell lines and expression of B-cell lymphoma 2 (Bcl-2) and phosphatase and tensin homolog (Pten). Four leukemic cell lines (HL-60, U937, Raji, and K562) were treated with 0, 1, 5, 10, and 20 ng/mL TIEG1, respectively. The cell growth inhibitory ratio was assessed using the MTT assay. An inhibitory curve was drawn, and half-maximal inhibitory concentration was calculated. Additionally, 1640 culture medium containing 10 ng/mL TIEG1 was used to culture leukemic cell lines for 0, 6, 12, 24, and 48 h. The apoptosis of each cell line at different time points was detected by flow cytometry. Total RNA was extracted before reverse transcription-polymerase chain reaction. The products of this reaction were analyzed by electrophoresis, and the expression of Bcl-2/Bcl-2-associated X protein (Bax) and Pten were detected. After treatment with TIEG1, proliferation of the 4 leukemic cell lines was inhibited both time-and dose-dependently. During apoptosis induction, the expression of Bcl-2 was decreased and the expressions of Bax and Pten were increased in the 4 leukemic cell 1969 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (1): 1968-1974 (2015 Effect of TIEG1 on leukemic cells lines induced by TIEG1 (P < 0.05). TIEG1 can inhibit the proliferation of leukemic cells and induce their apoptosis in a time-and dosedependent manner. A close relationship exists between Bcl-2/Bax and Pten expression and cell apoptosis induced by TIEG1.

TIEG1 deficiency confers enhanced myocardial protection in the infarcted heart by mediating the Pten/Akt signalling pathway

“…Bcl-2 and Bax are relevant to apoptosis in CMs, and they are apoptosis involved factors in myocytes under ischaemic conditions (29,30). A correlation between TIEG1 and Bcl/Bax in tumour cells has been confirmed (12); however, this remains unclear in cardiovascular cells.…”

“…A number of studies have revealed the biological functions of TIEG1 in different cells (12,15,21). Of these properties, apoptosis induction and proliferation inhibition by TIEG1 have garnered attention from researchers.…”

“…Jin et al found that TIEG1 is a key regulator that promotes the apoptosis of K562 leukaemic cells (25). Furthermore, TIEG1 has been shown to promote the apoptosis of different leukaemia cell lines, such as HL-60, U937, Raji and K562, in a dose- and time-dependent manner (12). For cardiovascular diseases, TIEG1 was first reported to be involved in cardiac hypertrophy in 2007 (26), and this result was confirmed in a later clinic study (27).…”

“…There has been significant progress regarding the role of TIEG1 in various diseases. In the field of cancer studies, Yao et al found that TIEG1 blocked the proliferation and induced the apoptosis of leukaemic cell lines, including HL-60, U937, Raji and K562 in both a time- and dose-dependent manner (12). Jiang et al proved that the transactivation of TIEG1 inhibited the growth of hepatocellular carcinoma cells in a dose-dependent manner (13).…”

Ozone alleviates ischemia/reperfusion injury by inhibiting mitochondrion‐mediated apoptosis pathway in SH‐SY5Y cells

“…Bcl‐2 could promote cell survival, but Bax could promote cell death by apoptosis. The ratio of Bcl‐2/Bax is a key factor that decides whether or not apoptosis happens to cells after injuries (Liang et al, 2013; Yao et al, 2015). Some reports indicated that the caspase family could promote and implement cell apoptosis, and caspase‐3 is the most important downstream protease (Prabhakar et al, 2003; Fianco et al, 2016).…”