Transmembrane protein 160 (TMEM160)

Transmembrane protein 160 (TMEM160) is a mitochondrial inner membrane protein involved in modulating mitochondrial stress responses and limiting the production of reactive oxygen species (ROS)[1][4]. It plays a protective role in mitochondrial proteostasis by suppressing mitochondrial unfolded protein response (UPRmt) and maintaining redox balance[1]. In cancer, TMEM160 promotes growth, immune evasion, radioresistance, and resistance to ferroptosis by enhancing degradation of KEAP1 and activating the NRF2/GPX4/SLC7A11 axis[2]. Its knockdown results in increased sensitivity to oxidative damage and ferroptotic cell death. TMEM160 has emerged as a novel cancer progression and drug resistance target, but extensive clinical targeting of this molecule is not yet established[2]. TMEM160 is a mitochondrial transmembrane protein newly identified as a regulator of oxidative stress responses and ferroptosis, with emerging roles in cancer biology and therapeutic resistance, but it is not a classical receptor, enzyme, or ion channel[1][2][4]. There are no approved drugs for TMEM160, but its expression and function provide novel biomarker and therapeutic potential.

Other names

TMEM160FLJ20512transmembrane protein 160

For experimental agents: TMEM160 knockdown sensitizes cells to erastin-induced ferroptosis; inhibition or loss of TMEM160 increases cell death via ferroptosis, and Ferrostatin-1 can rescue this effect. TMEM160 promotes cancer cell chemoresistance by activating the NRF2-GPX4 pathway via KEAP1 degradation.