Dual Targeting of v-ATPase and mTORC1 Signaling Disarms Multidrug-Resistant Cancers

Tayah Turocy; Jason M Crawford

doi:10.1016/j.chembiol.2020.10.013

Dual Targeting of v-ATPase and mTORC1 Signaling Disarms Multidrug-Resistant Cancers

Cell Chem Biol. 2020 Nov 19;27(11):1329-1331. doi: 10.1016/j.chembiol.2020.10.013.

Authors

Tayah Turocy¹, Jason M Crawford²

Affiliations

¹ Department of Chemistry, Yale University, New Haven, CT 06520, USA; Chemical Biology Institute, Yale University, West Haven, CT 06516, USA.
² Department of Chemistry, Yale University, New Haven, CT 06520, USA; Chemical Biology Institute, Yale University, West Haven, CT 06516, USA; Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06536, USA. Electronic address: [email protected].

PMID: 33217311
DOI: 10.1016/j.chembiol.2020.10.013

Abstract

Chemotherapeutic treatments are frequently impeded by the development of multidrug resistance (MDR). In this issue of Cell Chemical Biology, Wang et al. (2020) identify the natural product verucopeptin as having therapeutic potential toward MDR cancer cell types by targeting v-ATPase and mTORC1 signaling.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Comment

MeSH terms

Antineoplastic Agents* / pharmacology
Drug Resistance, Multiple / drug effects
Drug Resistance, Neoplasm / drug effects
Mechanistic Target of Rapamycin Complex 1
Neoplasms* / drug therapy
Vacuolar Proton-Translocating ATPases* / pharmacology

Substances

Antineoplastic Agents
Mechanistic Target of Rapamycin Complex 1
Vacuolar Proton-Translocating ATPases

Abstract

Publication types

MeSH terms

Substances

Grants and funding