@article{oai:repo.qst.go.jp:00046768,
 author = {Gao, Jianchao and Aslam, Khan Ammad and Shimokawa, Takashi and Zhan, Jun and Strömblad, Staffan and Fang, Weigang and Zhang, Hongquan and 下川 卓志},
 issue = {6},
 journal = {FEBS letters},
 month = {Mar},
 note = {Kindlin-2 is engaged in tumor progression. However, the mechanism accounting for Kindlin-2 regulation in tumor cells remained largely unknown. Here, we report a regulatory loop between Kindlin-2 and GLI1, an effector of Hedgehog signaling pathway. We show that Kindlin-2 is transcriptionally downregulated via GLI1 occupancy on the Kindlin-2 promoter. Adversely, we found that Kindlin-2 promotes GLI1 expression through a mechanism involving GSK3β inactivation and is independent of Smoothened. Functionally, knockdown of Kindlin-2 cooperates with cyclopamine, a Smoothened antagonist, to decrease the viability of prostate cancer cells. Taken together, targeting the Kindlin-2-GLI1 feedback loop may facilitate the killing of prostate cancer cells.},
 title = {A feedback regulation between Kindlin-2 and GLI1 in prostate cancer cells.},
 volume = {587},
 year = {2013}
}