AI Article Synopsis
- Hepatocellular carcinoma (HCC) significantly impacts global health due to its high rates of occurrence and death.
- Osteopontin (OPN), a protein found at elevated levels in various cancers, including HCC, contributes to tumor growth, chemotherapy resistance, and the maintenance of stem-like traits in cancer cells.
- Research indicates that OPN promotes autophagy, which enhances cancer cell survival and resistance to treatment, suggesting that targeting OPN could be a potential strategy for improving HCC therapy.
Article Abstract
Hepatocellular carcinoma (HCC) is a major health burden worldwide for its high incidence and mortality. Osteopontin (OPN) is a chemokine-like, matricellular phosphoglycoprotein whose expression is elevated in various types of cancer including HCC. OPN has been shown to be involved in tumorigenesis, chemo-resistance, metastasis and sustaining stem-like properties of cancer cells. Autophagy is a cellular process by which cytoplasmic components are degraded and recycled for maintaining cellular homeostasis. There is increasing evidence supports that autophagy plays a critical role for stem-like properties and chemo-resistance of cancer cells. However, the relationship between OPN and autophagy in maintaining cancer stem-like properties and chemo-resistance is yet to be clarified. Herein, we found that secreted OPN induced autophagy via binding with its receptor integrin αvβ3 and sustaining FoxO3a stability. OPN-elicited autophagy could promote cancer cell survival and resistance to chemotherapy drugs, as well as stem-like properties. Our findings indicated that OPN was capable of promoting chemo-resistance of HCCs via autophagy, which might provide a new strategy for the treatment of HCC.
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| http://dx.doi.org/10.1016/j.canlet.2016.09.033 | DOI Listing |
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