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Mucins reprogram stemness, metabolism and promote chemoresistance during cancer progression

期刊

CANCER AND METASTASIS REVIEWS
卷 40, 期 2, 页码 575-588

出版社

SPRINGER
DOI: 10.1007/s10555-021-09959-1

关键词

Mucins; Cancer stem cell; Chemoresistance; Epithelial to mesenchymal transition; Metabolic reprogramming; Metastasis

类别

资金

  1. National Institutes of Health [P01 CA217798, R01 CA210637, R01 CA183459, R01 CA195586, R01 CA201444, R01 CA228524, F99 CA234962, U01 CA200466, U01 CA210240]
  2. Nebraska Department of Health and Human Services [LB595]

向作者/读者索取更多资源

Mucins play a crucial role in aggressive cancers by regulating disease progression, tumor proliferation, and chemotherapy resistance. They also contribute to the epithelial to mesenchymal transition (EMT) of cancer cells and enriching and maintaining the cancer stem cell (CSC) population, leading to chemoresistance and tumor progression. Additionally, mucins are involved in metabolic reprogramming during oncogenesis and cancer progression, influencing tumor cell survival, proliferation, and resistance to drugs.
Mucins are high-molecular-weight glycoproteins dysregulated in aggressive cancers. The role of mucins in disease progression, tumor proliferation, and chemotherapy resistance has been studied extensively. This article provides a comprehensive review of mucin's function as a physical barrier and the implication of mucin overexpression in impeded drug delivery to solid tumors. Mucins regulate the epithelial to mesenchymal transition (EMT) of cancer cells via several canonical and non-canonical oncogenic signaling pathways. Furthermore, mucins play an extensive role in enriching and maintaining the cancer stem cell (CSC) population, thereby sustaining the self-renewing and chemoresistant cellular pool in the bulk tumor. It has recently been demonstrated that mucins regulate the metabolic reprogramming during oncogenesis and cancer progression, which account for tumor cell survival, proliferation, and drug-resistance. This review article focuses on delineating mucin's role in oncogenic signaling and aberrant regulation of gene expressions, culminating in CSC maintenance, metabolic rewiring, and development of chemoresistance, tumor progression, and metastasis.

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