Deciphering the role of Hippo pathway in lung cancer

Hippo pathway has been initially recognized as a regulatory mechanism for modulation of organ size in fruitfly. Subsequently, its involvement in the regulation of homeostasis and tumorigenesis has been identified. This pathway contains some tumor suppressor genes such as hippo (hpo) and warts (wts), as well as a number of oncogenic ones such as yorkie (yki). Recent studies have shown participation of Hippo pathway in the lung carcinogenesis. This pathway can affect lung cancer via different mechanisms. The interaction between some miRNAs and Hippo pathway is a possible mechanism for carcinogenic processes. Moreover, some other types of non-coding RNAs including PVT1, SFTA1P, NSCLCAT1 and circ_0067741 are implicated in this process. Besides, anti-cancer effects of gallic acid, icotinib hydrochloride, curcumin, ginsenoside Rg3, cryptotanshinone, nitidine chloride, cucurbitacin E, erlotinib, verteporfin, sophoridine, cisplatin and verteporfin in lung cancer are medi-ated through modulation of Hippo pathway. Here, we summarize the results of recent studies that investigated the role of Hippo signaling in the progression of lung cancer, the impact of non-coding RNAs on this pathway and the effects of anti-cancer agents on Hippo signaling in the context of lung cancer.

Automated summary

The Hippo pathway plays a crucial role in regulating organ size, homeostasis, and tumorigenesis. It is involved in lung carcinogenesis through various mechanisms, including the interaction between miRNAs and the Hippo pathway. Non-coding RNAs such as PVT1, SFTA1P, NSCLCAT1, and circ_0067741 are also implicated in this process. Furthermore, several anti-cancer agents can modulate the Hippo pathway to exert their anti-cancer effects in lung cancer. This article summarizes recent studies on the role of Hippo signaling in lung cancer progression, the impact of non-coding RNAs on this pathway, and the effects of anti-cancer agents.