Src family kinase inhibitor PP2 efficiently inhibits cervical cancer cell proliferation through down-regulating phospho-Src-Y416 and phospho-EGFR-Y1173

@article{Kong2011SrcFK,
  title={Src family kinase inhibitor PP2 efficiently inhibits cervical cancer cell proliferation through down-regulating phospho-Src-Y416 and phospho-EGFR-Y1173},
  author={Lu Kong and Zhihong Deng and Haiying Shen and Yuxiang Zhang},
  journal={Molecular and Cellular Biochemistry},
  year={2011},
  volume={348},
  pages={11-19}
}
Tyrosine (Y) kinases inhibitors have been approved for targeted treatment of cancer. However, their clinical use is limited to some cancers and the mechanism of their action remains unclear. Previous study has indicated that PP2, a selective inhibitor of the Src family of non-receptor tyrosine kinases (nRTK), efficiently repressed cervical cancer growth in vitro and in vivo. In this regard, our aims are to explore the mechanism of PP2 on cervical cancer cell growth inhibition by investigating… 
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37 Citations

Bosutinib Acts as a Tumor Inhibitor via Downregulating Src/NF‐κB/Survivin Expression in HeLa Cells

Bosutinib, as a potent dual Src/Abl inhibitor, could exert anti‐tumor effects on cervical cancer and inhibited cervical cancer cells proliferation and colony formation ability in a dose‐dependent manner, and also induced apoptosis.

Janus kinases and Src family kinases in the regulation of EGF-induced vimentin expression in MDA-MB-468 breast cancer cells.

Src family kinase inhibitor PP2 accelerates differentiation in human intestinal epithelial cells.

c-Src inhibitor PP2 inhibits head and neck cancer progression through regulation of the epithelial-mesenchymal transition.

PP2 inhibits cell growth and progression in HNSCC by regulating the epithelial-mesenchymal transition pathway downstream of c-Src.

Thymoquinone induces apoptosis in human colon cancer HCT116 cells through inactivation of STAT3 by blocking JAK2- and Src‑mediated phosphorylation of EGF receptor tyrosine kinase.

TQ induced apoptosis in HCT116 cells by blocking STAT3 signaling via inhibition of JAK2- and Src-mediated phosphorylation of EGFR tyrosine kinase.

SRC kinase family inhibitor PP2 promotes DMSO-induced cardiac differentiation of P19 cells and inhibits proliferation.

Epidermal growth factor promotes cyclin G2 degradation via calpain-mediated proteolysis in gynaecological cancer cells

It is demonstrated that EGF-induced, calpain-mediated proteolysis contributes to the rapid destruction of cyclin G2 and that the PEST domain is critical for EGF/calpain actions.

Activation of Src, Fyn and Yes non-receptor tyrosine kinases in keratinocytes expressing human papillomavirus (HPV) type 16 E7 oncoprotein

This study revealed that HPV 16 oncoproteins upregulate Src family kinases Src and Yes via posttranscriptional mechanisms and enhances the activating phosphorylation of SFKs expressed in keratinocytes.

Growth inhibitory effect of the Src inhibitor dasatinib in combination with anticancer agents on uterine cervical adenocarcinoma cells

Src is overexpressed in cervical adenocarcinoma cell lines, and dasatinib inhibits intracellular Src signaling and causes apoptosis, and the results suggest that Src may be targeted in novel therapeutic strategies for cervicalAdenocARCinoma.

SMAD4-independent activation of TGF-β signaling by MUC1 in a human pancreatic cancer cell line

Data strongly suggests that MUC1 may regulate TGF-β function in PDA cells and thus have potential clinical relevance in the use of T GF-β inhibitors in clinical trials.

References

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Immunohistochemical and confocal microscope studies suggested that pSrcY416 is overexpressed in HeLa and SiHa cells, as well as in the clinical cervical cancer tissues, compared to the normal cervical tissues, and nrTKs could be a novel therapeutic targets for the treatment of cervical cancer.

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It is demonstrated that PP1, a pharmacological inhibitor of Src kinases, blocked SCF-mediated activation of mitogen-activated protein (MAP) kinase, but it also inhibited Kit activation, which suggests that the SCF/Kit autocrine loop, through activation of Lck and subsequently MAP kinase and the mutational inactivation of Rb contribute to the loss of G1-S phase checkpoint regulation during the pathogenesis of SCLC.