Selective form of autophagy for cellular quality control ( 6).

Systemic therapies, only ~50% of patients with CRC survive for atĬhemotherapeutic drugs can significantly inhibit the progression ofĬRC, but drug resistance remains a major cause of failure inĬhaperone-mediated autophagy (CMA) is a highly Process and the molecular mechanisms of its development andĪlthough some improvements have been made in early diagnosis and Thus, CMA is a promising predictor of chemosensitivity to 5‑FU treatment and anti‑CMA therapy may be a novel therapeutic option for patients with CRC.Ĭolorectal cancer (CRC) is one of the most frequentĬauses of cancer-related deaths worldwide ( 1). Taken together, the results of the present study suggested that chemoresistance in patients with CRC may be mediated by enhancing CMA. Accordingly, loss or gain of function of LAMP2A in 5‑FU‑resistant CRC cells rendered them sensitive or resistant to 5‑FU, respectively. High expression of LAMP2A was found to be responsible for 5‑FU resistance and to enhance PLD2 expression through the activation of NF‑κB pathway. In engineered 5‑FU‑resistant CRC cell lines, a significant elevation of lysosome‑associated membrane protein 2A (LAMP2A), which is the key molecule in the CMA pathway, was identiﬁed. The present study investigated the mechanisms underlying the response and resistance to 5‑fluorouracil (5‑FU) in colorectal cancer (CRC) cell lines. Chaperone‑mediated autophagy (CMA) is a selective type of autophagy whereby a specific subset of intracellular proteins is targeted to the lysosome for degradation.

Chaperone mediated autophagy assays