miR-33b in human cancer: Mechanistic and clinical perspectives

Wenlong Zhang; Bincan Jiang; Hecheng Zhu; Ailan Cheng; Can Li; Haoxuan Huang; Xuewen Li; Yirui Kuang

doi:10.1016/j.biopha.2023.114432

miR-33b in human cancer: Mechanistic and clinical perspectives

Biomed Pharmacother. 2023 May:161:114432. doi: 10.1016/j.biopha.2023.114432. Epub 2023 Feb 24.

Authors

Wenlong Zhang¹, Bincan Jiang², Hecheng Zhu³, Ailan Cheng², Can Li¹, Haoxuan Huang¹, Xuewen Li³, Yirui Kuang⁴

Affiliations

¹ Department of Neurosurgery, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, China; Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha, Hunan Province, 410008, China.
² Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, Hunan Province, 421001, China.
³ Changsha Kexin Cancer Hospital, Changsha, Hunan Province 410205, China.
⁴ Department of Neurosurgery, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, China; Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha, Hunan Province, 410008, China. Electronic address: philkyr@163.com.

PMID: 36841026
DOI: 10.1016/j.biopha.2023.114432

Abstract

The microRNAs (miRNAs), an extensive class of small noncoding RNAs (∼22 nucleotides), have been shown to have critical functions in various biological processes during development. miR-33b (or hsa-miR-33b) is down-regulated in cancer of multiple systems. Notably, at least 27 protein-coding genes can be targeted by miR-33b. miR-33b regulates the cell cycle, cell proliferation, various metabolism pathways, epithelial-mesenchymal transition (EMT), cancer cell invasion and migration, etc. In prostate cancer, Cullin 4B (CUL4B) can be recruited to the promoter to inhibit the expression of miR-33b. In gastric cancer, the hypermethylation of the CpG island regulated the expression of miR-33b. Besides, miR-33b could be negatively regulated by 7 competing-endogenous RNAs (ceRNAs), which are all long non-coding RNAs (lncRNAs). There are at least 4 signaling pathways, including NF-κB, MAP8, Notch1, and Wnt/β-catenin signaling pathways, which could be regulated partially by miR-33b. Additionally, low expression of miR-33b was associated with clinicopathology and prognosis in cancer patients. In addition, the aberrant expression of miR-33b was connected with the resistance of cancer cells to 5 anticancer drugs (cisplatin, docetaxel, bortezomib, paclitaxel, and daunorubicin). Importantly, our work systematically summarizes the aberrant expression of miR-33b in various neoplastic diseases and the effect of its downregulation on the biological behavior of cancer cells. Furthermore, this review focuses on recent advances in understanding the molecular regulation mechanisms of miR-33b. Moreso, the relationship between the miR-33b expression levels and the clinicopathological data and prognosis of tumor patients was summarized for the first time. Overall, we suggest that the current studies of miR-33b are insufficient but provide potential hints and direction for future miR-33b-related research.

Keywords: Biomarker; CeRNA; Drug; Mechanisms; MiR-33b; Prognosis.

Publication types

Review

MeSH terms

Antineoplastic Agents* / pharmacology
Antineoplastic Agents* / therapeutic use
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cisplatin / metabolism
Cullin Proteins / metabolism
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Humans
Male
MicroRNAs* / genetics
MicroRNAs* / metabolism
RNA, Long Noncoding*
Stomach Neoplasms* / pathology
Wnt Signaling Pathway

Substances

MicroRNAs
Cisplatin
Antineoplastic Agents
RNA, Long Noncoding
CUL4B protein, human
Cullin Proteins