2024-03-29T13:31:40Zhttp://uvadoc.uva.es/oai/requestoai:uvadoc.uva.es:10324/450282021-06-24T07:16:30Zcom_10324_44585com_10324_954com_10324_894col_10324_44586
00925njm 22002777a 4500
dc
Villalobos Jorge, Carlos
author
Sobradillo Luengo, Diego
author
Hernández Morales, Miriam
author
Núñez Llorente, Lucía
author
2017
Colorectal cancer (CRC) is the third most frequent form of cancer and the fourth leading cause of cancer-related death in the world. Basic and clinical data indicate that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) may prevent colon cancer but mechanisms remain unknown. Aspirin metabolite salicylate and other NSAIDs may inhibit tumor cell growth acting on store-operated Ca2 + entry (SOCE), suggesting an important role for this pathway in CRC. Consistently, SOCE is emerging as a novel player in different forms of cancer, including CRC. SOCE and store-operated currents (SOCs) are dramatically enhanced in CRC while Ca2 + stores are partially empty in CRC cells. These features may contribute to CRC hallmarks including enhanced cell proliferation, migration, invasion and survival. At the molecular level, enhanced SOCE and depleted stores are mediated by overexpression of Orai1, Stromal interaction protein 1 (STIM1) and Transient receptor protein channel 1 (TRPC1) and downregulation of STIM2. In normal colonic cells, SOCE is mediated by Ca2 +-release activated Ca2 + channels made of STIM1, STIM2 and Orai1. In CRC cells, SOCE is mediated by different store-operated currents (SOCs) driven by STIM1, Orai1 and TRPC1. Loss of STIM2 contributes to depletion of Ca2 + stores and enhanced resistance to cell death in CRC cells. Thus, SOCE is a novel key player in CRC and inhibition by salicylate and other NSAIDs may contribute to explain chemoprevention activity.
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2017, vol. 1864, n. 6. p. 843-849
0167-4889
http://uvadoc.uva.es/handle/10324/45028
10.1016/j.bbamcr.2017.01.005
Calcium remodeling in colorectal cancer