Hippo Signaling in Cancer: Lessons from Drosophila Models
- 1Department of Biology, College of Arts and Sciences, University of Dayton, United States
- 2College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, United States
- 3Integrative Science and Engineering Center, College of Arts and Sciences, University of Dayton, United States
- 4University of Dayton, United States
Hippo pathway was initially identified through genetic screens for genes regulating organ size in fruitflies. Recent studies have highlighted the role of Hippo signaling as a key regulator of homeostasis, and in tumorigenesis.. Hippo pathway is comprised of genes that act as tumor suppressor genes like hippo (hpo) and warts (wts), and oncogenes like yorkie (yki). YAP and TAZ are two related mammalian homologs of Drosophila Yki that act as effectors of the Hippo pathway. Hippo signaling deficiency can cause YAP- or TAZ-dependent oncogene addiction for cancer cells. YAP and TAZ are often activated in human malignant cancers. These transcriptional regulators may initiate tumorigenic changes in solid tumors by inducing cancer stem cells and proliferation, culminating in metastasis and chemo-resistance. Given the complex mechanisms (e.g., of the cancer microenvironment, and the extrinsic and intrinsic cues) that overpower YAP/TAZ inhibition, the molecular roles of the Hippo pathway in tumor growth and progression remain poorly defined. Here we review recent findings from studies in whole animal model organism like Drosophila on the role of Hippo signaling regarding its connection to inflammation, tumor microenvironment, and other oncogenic signaling in cancer growth and progression.
Keywords: Drosophila, Hippo pathway, Cell Proliferation, Cell Death, Cancer, Cell Polarity, Oncogenic cooperation
Received: 04 Mar 2019;
Accepted: 03 May 2019.
Edited by:SrinivasVinod Saladi, Massachusetts Eye & Ear Infirmary, Harvard Medical School, United States
Reviewed by:Rizaldy P. Scott, Division of Nephrology & Hypertension, Feinberg School of Medicine, Northwestern University, United States
Sirisha M. Cheedipudi, University of Texas Health Science Center at Houston, United States
Copyright: © 2019 Snigdha, Gangwani, Lapalikar, Singh and Kango-Singh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Madhuri Kango-Singh, Department of Biology, College of Arts and Sciences, University of Dayton, Dayton, Nevada, United States, email@example.com