Furthermore, TUNEL+ cells and the relative caspase-3 activity in the CC cells were increased in the RT/BE group compared to those in the RT alone group.
Moreover, knockdown of <i>Lnc-IL7R</i> by two different siRNAs in cervical cancer cell lines Hela and SiHa induced impaired cell vitality and caspase-3-dependent apoptosis <i>in vitro</i> Furthermore, inhibition of <i>Lnc-IL7R in vivo</i> significantly restricted the tumor growth with decreased expressions of proliferation index Ki-67 and <i>Lnc-IL7R</i> These data indicated that <i>Lnc-IL7R</i> predicts a poor clinical outcome of cervical cancer patients, and knockdown of <i>Lnc-IL7R</i> is amenable to the treatment of cervical cancer.
Clonogenic assay, PCNA staining, TUNEL staining and caspase-3 activity assay were used to investigate the direct in vitro effect of T. Vag on human cervical cancer by using HeLa cells.
These data indicate that through upregulating the expression of caspase-3, the TT genotype of caspase-3rs1049216 can be associated with not only the risk of cervical cancer but also the progression of this cancer.
Moreover, α-mangostin also repressed tumor growth in accordance with increased levels of p-ASK1, p-p38, cleaved-PARP and cleaved-caspase-3 in the tumor mass from the mouse xenograft model of cervical cancer.
CONCLUSIONS Our results suggest that overexpression of miR-148b protects against cervical cancer by inducing G1/S-phase cell cycle arrest and apoptosis through caspase-3-dependent manner, and overexpression of miR-148b might develop a therapeutic intervention for cervical cancer.
Up-regulation of ENST00000420168, ENST00000564977 and down-regulation of TCONS_00010232 might stimulate FOXQ1 expression and suppress CASP3 expression in HPV-18 positive cervical cancer cell, which lead to HPV-induced proliferation and deficiency in apoptosis.
Significant improvement of XIAP gene silencing and cleaved caspase-3 activation was achieved, resulting in good therapeutic effect on human cervical cancer xenograft model in nude mice.
Therefore, our research revealed the mechanistic links between miR-744 and Bcl-2 in the pathogenesis of cervical cancer through modulation of Caspase-3, leading to the inhibition of cervical cancer cell growth.
Our data demonstrated that MALAT1 was involved in cervical cancer cell growth, cell cycle progression, and invasion through the regulation of gene expression, such as caspase-3, -8, Bax, Bcl-2, and BclxL, suggesting that MALAT1 could have important implications in cervical cancer biology.
Stable transfer of the extrinsic Smac gene and its over-expression in cervical cancer cell line could significantly enhance the expression and activities of cellular caspase-3 and ameliorate apoptosis-inducing effects of irradiation on cancer cells, which was a novel strategy to improve radiotherapeutic effects on cervical cancer.