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Inhibition of the sarco/endoplasmic reticulum (ER) Ca²⁺-ATPase by thapsigargin analogs induces cell death via ER Ca²⁺ depletion and the unfolded protein response.

ABSTRACT: Calcium (Ca²⁺) is a fundamental regulator of cell signaling and function. Thapsigargin (Tg) blocks the sarco/endoplasmic reticulum (ER) Ca²⁺-ATPase (SERCA), disrupts Ca²⁺ homeostasis, and causes cell death. However, the exact mechanisms whereby SERCA inhibition induces cell death are incompletely understood. Here, we report that low (0.1 μm) concentrations of Tg and Tg analogs with various long-chain substitutions at the O-8 position extensively inhibit SERCA1a-mediated Ca²⁺ transport. We also found that, in both prostate and breast cancer cells, exposure to Tg or Tg analogs for 1 day caused extensive drainage of the ER Ca²⁺ stores. This Ca²⁺ depletion was followed by markedly reduced cell proliferation rates and morphologic

SUBMITTER: Sehgal P

PROVIDER: S-EPMC5712609 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Inhibition of the sarco/endoplasmic reticulum (ER) Ca²⁺-ATPase by thapsigargin analogs induces cell death via ER Ca²⁺ depletion and the unfolded protein response.

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Inhibition of the sarco/endoplasmic reticulum (ER) Ca2+-ATPase by thapsigargin analogs induces cell death via ER Ca2+ depletion and the unfolded protein response.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Inhibition of the sarco/endoplasmic reticulum (ER) Ca²⁺-ATPase by thapsigargin analogs induces cell death via ER Ca²⁺ depletion and the unfolded protein response.