Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma

Version 1 : Received: 31 January 2020 / Approved: 3 February 2020 / Online: 3 February 2020 (05:20:36 CET)

A peer-reviewed article of this Preprint also exists.

Perez-Montoyo, H. Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma. Cells 2020, 9, 614. Perez-Montoyo, H. Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma. Cells 2020, 9, 614.


Autophagy is a multistep catabolic process through which misfolded, aggregated or mutated proteins and damaged organelles are internalized in membrane vesicles called autophagosomes and ultimately fused to lysosomes for degradation of sequestered components. The multi-step nature of the process offers multiple regulation points prone to be deregulated and cause different human disease, but also offers multiple targetable points for designing therapeutic strategies. Cancer cells have evolved to use autophagy as an adaptive mechanism to survive under extremely stressful conditions within tumor microenvironment, but also to increase invasiveness and resistance to anti-cancer drugs such as chemotherapy. This review collects all clinical evidences of autophagy deregulation during cholangiocarcinogenesis together with all pre-clinical reports evaluating compounds that modulate autophagy to induce cholangiocarcinoma (CCA) cell death. Altogether, experimental data suggests an impairment of autophagy during initial steps of CCA development and increased expression of autophagy markers on established tumors and in invasive phenotypes. Pre-clinical efficacy of autophagy modulators promoting CCA cell death, reducing invasiveness capacity and resensitizing CCA cells to chemotherapy open novel therapeutic avenues to design more specific and efficient strategies to treat this aggressive cancer


cholangiocarcinoma; autophagy inhibition; autophagy inhibition; chemoresistance


Medicine and Pharmacology, Oncology and Oncogenics

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