Expression of Apoptosis-Associated Proteins in Tumor Cells under Autophagy and Endoplasmic Reticulum Stress Stimulation in Mouse Skin Melanoma Model.

Iu S Taskaeva, I S Gogaeva, N P Bgatova

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Article in Bulletin of experimental biology and medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 authors.

Iu S TaskaevaResearch Institute of Clinical and Experimental Lymphology - Branch of Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia. inabrite@yandex.ru.

I S GogaevaResearch Institute of Clinical and Experimental Lymphology - Branch of Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia.

N P BgatovaResearch Institute of Clinical and Experimental Lymphology - Branch of Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The autophagy-related structures, the size of the rough endoplasmic reticulum (ER) cisterns, and the expression of apoptosis-related proteins were assessed by transmission electron microscopy and immunohistochemistry in tumor samples from mice with B16 skin melanoma after administration of autophagy inducer (rapamycin) or ER stress inducer (brefeldin A). Brefeldin A stimulated significant ER stress in mouse skin melanoma cells, but rapamycin contributed to the maintenance of cell homeostasis by inducing autophagy, which was confirmed by the presence of autophagy-related structures and significantly smaller sizes of the rough ER cisterns in the group of mice receiving both rapamycin and brefeldin A. Brefeldin A-induced ER stress triggered apoptosis of tumor cells. Moreover, simultaneous stimulation of autophagy and ER stress in tumor cells promoted cytoprotective selective autophagy (reticulophagy) aimed at resolving ER stress, which may be a mechanism underlying the development of chemoresistance in skin melanoma.

Indexed as

AutophagyEndoplasmic Reticulum StressMelanoma, ExperimentalSkin NeoplasmsAnimalsApoptosisBrefeldin ACell Line, TumorDisease Models, AnimalMelanomaMiceMice, Inbred C57BLSirolimusBrefeldin ASirolimusautophagychemoresistanceendoplasmic reticulum stressskin melanoma

Identifiers

PMID41186825

DOI10.1016/j.molcel.2008.11.014

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