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IMPA2 blocks cervical cancer cell apoptosis and induces paclitaxel resistance through p53-mediated AIFM2 regulation
Ist Teil von
Acta biochimica et biophysica Sinica, 2023-04, Vol.55 (4), p.623-632
Ort / Verlag
China: China Science Publishing & Media Ltd
Erscheinungsjahr
2023
Link zum Volltext
Quelle
EZB-FREE-00999 freely available EZB journals
Beschreibungen/Notizen
Cervical cancer continues to be a concern, and the prognosis of locally advanced cervical cancer remains poor.
was previously identified as a potential oncogene and regulator of tumor apoptosis. In this study, we aim to further elucidate the underlying mechanisms of
gene in the regulation of cervical cancer apoptosis. First, we identify
as an upregulated gene in
-silenced cervical cancer cells, and inhibition of
reverses
knockdown-induced apoptosis. Further study reveals that
regulates cell apoptosis in a mitochondrial-dependent manner with a redistribution of mitochondrial membrane potential and intracellular Ca
levels. However, the analysis of the STRING database and our experimental results show that
has little effect on cervical cancer progression and survival. Further mechanistic study demonstrates that
and
silencing inhibits apoptosis by activating p53. Meanwhile, the knockdown of
enhances the chemosensitivity of cervical cancer cells by strengthening paclitaxel-induced apoptosis. Based on the above results, the IMPA2/AIFM2/p53 pathway may be a new molecular mechanism for paclitaxel treatment of cervical cancer and an effective strategy to enhance the sensitivity of cervical cancer cells to paclitaxel. Our findings display a novel function of
in regulating cell apoptosis and paclitaxel resistance mediated by a disturbance of
and
expression, potentially making it a novel therapeutic target for cervical cancer treatment.