2002
DOI: 10.3892/ijo.20.4.723
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Bax-induction alone is sufficient to activate apoptosis cascade in wild-type Bax-bearing K562 cells, and the initiation of apoptosis requires simultaneous caspase activation

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Cited by 6 publications
(6 citation statements)
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“…The present study did not find any change in Bcl-2, an antiapoptotic protein, expression but levels of Bax, which is a proapoptotic protein, were lower in the PD-ECGF/TP-treated group than in pCI or Saline groups. It has been shown that the Bax protein, when present above a threshold level, triggers the apoptosis cascade (16). Our data also suggest that direct myocardial injection of the PD-ECGF/TP gene inhibited myocardial apoptosis, but the mechanism is not clear, whether it is via inhibiting Bax expression should be discussed further.…”
Section: Discussionmentioning
confidence: 84%
“…The present study did not find any change in Bcl-2, an antiapoptotic protein, expression but levels of Bax, which is a proapoptotic protein, were lower in the PD-ECGF/TP-treated group than in pCI or Saline groups. It has been shown that the Bax protein, when present above a threshold level, triggers the apoptosis cascade (16). Our data also suggest that direct myocardial injection of the PD-ECGF/TP gene inhibited myocardial apoptosis, but the mechanism is not clear, whether it is via inhibiting Bax expression should be discussed further.…”
Section: Discussionmentioning
confidence: 84%
“…This system is most suited, since previous studies demonstrated that tet-regulated overexpression of apoptotic genes mediates cell death in transfected cancer cells. Thus, tet-induced overexpression of BAX enhanced apoptosis induced by chemotherapeutic agents (Kobayashi et al, 2002). Similarly, Faris et al (1998) utilised the Tet-Off system for overexpression of a dominant-active MEKK1 molecule, which mediated apoptosis by upregulation of CD95-L.…”
Section: Discussionmentioning
confidence: 99%
“…Previously, we had shown that matrine treatment did not alter the expression of Bcl-xL, but up-regulated Bax protein level and caused the release of cytochrome C in K562 cells [25]. It has been reported that Bax-induction alone is sufficient to activate the apoptosis cascade in some cell types [26]. Our results imply that matrine may induce Bcl-2 and suppress Bax expression and thereby inhibit the growth of H22 hepatocarcinoma cells in vitro and in vivo but more work is required to further clarify the mechanisms of matrine-induced apoptosis.…”
mentioning
confidence: 90%