Introduction

MicroRNAs (miRNAs or miRs), 21–24 nucleotides in length, are small, single-stranded noncoding RNAs that regulate gene expression at the post-transcriptional level through target mRNA cleavage or translational inhibition. The process of their generaton is usually divided into two steps: (i) genomic DNA genetic information transcription by RNA polymerase II to produce primary miRNA(pri-miRNA) transcript, which contains one or a few stem-loop structures consisting of approximately 70 nucleotides each; and (ii) processing of pri-miRNA by a microprocessor, Dicer-like 1 protein, into precursor miRNA (pre-miRNA), which is also a stem-loop structure and finally becomes mature miRNA by modification [1]. The mature miRNA is incorporated into an RNA-induced silencing complex. They recognize target mRNAs through imperfect base pairing and commonly result in the translational inhibition or destabilization of the target mRNA.

Disclosing the biological functionality of miRNAs is generally implemented by animal knockout models and transgenic overexpression experiments [2]. Functional studies indicate that miRNAs regulate practically every cellular process investigated so far, such as cell proliferation, differentiation, immune response, metastasis, senescence, autophagy and apoptosis, via regulating housekee** genes and involving in various cell signaling pathways [3]. The changes in their expression are associated with many human pathologies [4,5,6]. The interesting thing is that the functions of miRNAs depend on different pathological types and physiological environments [3]. When miRNA is located in the cell plasma, it can act on the mRNA 3′-untranslated region (UTR) like a fire extinguisher, blocking the translation of mRNA and then exerting the negative regulation of genes. In contrast, when it is located in the nucleus, it serves as an igniter that changes the chromatin state of enhancers by binding to enhancers, thereby activating the transcriptional expression of genes.

The miR-34 family has been extensively studied and considered as tumor suppressor RNA because of its synergistic effect with the tumor suppressor p53 [7]. It is a tiny fragment located in the sub-band 1 of band 3 in the long arm 2 region of chromosome 11, including three members of miR-34a, miR-34b, and miR-34c. It is highly conserved during the evolutionary process. MiR-34 family acts as an antitumor agent by participating in some important signaling pathways or regulating multiple target mRNAs and proteins [8], such as phosphatidylinositol 3-kinase–protein kinase B signaling pathway (PI3K–Akt), Notch signaling pathway, cyclin dependent kinase (Cdk), and silent mating type information regulation 2 homolog 1 (SIRT1), promoting tumor cell apoptosis, inhibiting the proliferation and differentiation of tumor cells, hindering the invasion and migration of tumor cells, and enhancing immune surveillance [9]. In addition, recent studies have put forward that miR-34 family members not only assume the function of repressors in the development of tumors but also contribute to the pathogenesis of other diseases, such as regulating reproductive and nervous system function, influencing inflammatory and immune responses [10,11,12,65, 66]. TIMP3 was recognized as a direct target of miR-34b-5p in numerous studies since enhanced expression of miR-34b-5p led to a decline in TIMP3 expression and its knockdown was responsible for TIMP3 elevation. The research suggested that miR-34b-5p boosted bleomycin resistance by decreasing the expression of TIMP3 and further facilitated the fibrotic course of lung tissue [67].

A previous study showed a connection between idiopathic pulmonary arterial hypertension (IPAH) and and miR-34b-5p, which was associated with most of the declinable target differentially expressed genes, cell multiplication, and adhesion-independent growth [

Availability of data and materials

All data generated or analyzed during this study are included in this published article.

Abbreviations

miRNAs or miRs:

MicroRNAs

nt:

Nucleotides

pri-miRNA:

Primary miRNA

pre-miRNA:

Precursor miRNA

PDAC:

Pancreatic ductal adenocarcinoma

TNM:

Tumor-node-metastasis

circBFAR:

Circular-RNA BFAR

MET:

Mesenchymal–epithelial transition factor

OSCC:

Oral squamous cell carcinoma

CAC:

Colitis-associated cancer

CRC:

Colorectal cancer

BCL2:

B-cell lymphoma-2

ALI:

Acute lung injury

PGRN:

Progranulin

LPS:

Lipopolysaccharide

ECM:

Extracellular matrix

TIMP3:

Tissue inhibitor of metalloproteinases-3

BaP:

Benzo(a)pyrene

SCLC:

Small-cell lung cancer

BC:

Bladder carcinoma

AQP2:

Aquaporin-2

HK-2:

Human renal tubular epithelial cells

SSC:

Spermatogonial stem cell

PrM:

Premeiotic

EGME:

Ethylene glycol monomethyl ether

TH:

Testicular–hyperthermia

VEGF-A:

Vascular endothelial growth factor-A

ZEB1:

Zinc finger E-box-binding homeobox 1

EEC:

Endometrial endometrioid carcinoma

LNM:

Lymph node metastasis

MDA:

Minimal deviation adenocarcinoma

DEMs:

Differentially expressed miRNAs

CORT:

Corticosterone

DLBCL:

Diffuse large B-cell lymphoma

ALV-J:

Avian leukosis virus subgroup J

MDA5:

Melanoma differentiation-associated gene 5

IFN:

Interferon

FA:

Fluorine combined with aluminum

BDNF:

Brain-derived neurotrophic factor

PD:

Parkinson’s disease

SI:

Social isolation

MDD:

Major depressive disorder

IPAH:

Idiopathic pulmonary arterial hypertension

DEGs:

Differentially expressed genes

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Acknowledgements

We used the Microsoft PowerPoint software to produce the figures.

Funding

This study was supported by grants from the Natural Science Foundation of Jilin Province (Grant No.20200201438JC).

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  1. The Second Hospital of Jilin University, Changchun, Jilin, China

    Xuechun Bai, Lianwen Zheng, Ying Xu, Yan Liang & Dandan Li

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  1. Xuechun Bai
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  2. Lianwen Zheng
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  3. Ying Xu
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  4. Yan Liang
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  5. Dandan Li
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ZLW contributed to the conception and design of the study. XY and LY organized the database. BXC wrote the first draft of the manuscript. LDD wrote sections of the manuscript. All authors read and approved the final manuscript.

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Correspondence to Dandan Li.

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Bai, X., Zheng, L., Xu, Y. et al. Role of microRNA-34b-5p in cancer and injury: how does it work?. Cancer Cell Int 22, 381 (2022). https://doi.org/10.1186/s12935-022-02797-3

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