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. 2021 May 28;13(11):2649. doi: 10.3390/cancers13112649

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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PDIA1 inhibition by CCF642 analogues induce acute endoplasmic reticulum (ER) stress response and lead to apoptosis. Multiple myeloma cells (MM1.S) were treated with 3 µM of CCF642, -34, -37, -39, -34-A, and Tunicamycin (as a control). The status of ER sensors (XBP-1S, IRE1α oligomerization, and induction of C/EBP homology protein (CHOP)) along with apoptosis markers (cleaved caspase 3 and PARP1) were monitored. (A) MM1.S cells were treated for 4 h with CCF642 and its indicated analogues. (B) MM1.S cells were treated with CCF642-34 in a time course. (C) MM1.S, MM1.S.luc, and BTZ-resistant MM1.S.luc cells were stained with the H2DCFDA ROS detection and then treated with 2.5 µM CCF642-34 up to 4 h.