Determinants of Functional MicroRNA Targeting

Hwang, Hyeonseo; Chang, Hee Ryung; Baek, Daehyun

doi:10.14348/molcells.2023.2157

Cited by 19 publications

(7 citation statements)

References 158 publications

(221 reference statements)

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“…Numerous miRNAs have been found to have links to certain types of cancer [ 11 , 12 ]. Three observations made during the early stages of miRNA research suggested that they may play a role in human cancer.…”

Section: Mirnas and Cancermentioning

confidence: 99%

How MicroRNAs Command the Battle against Cancer

Wu,

Leng,

Sergi

et al. 2024

IJMS

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MicroRNAs (miRNAs) are small RNA molecules that regulate more than 30% of genes in humans. Recent studies have revealed that miRNAs play a crucial role in tumorigenesis. Large sets of miRNAs in human tumors are under-expressed compared to normal tissues. Furthermore, experiments have shown that interference with miRNA processing enhances tumorigenesis. Multiple studies have documented the causal role of miRNAs in cancer, and miRNA-based anticancer therapies are currently being developed. This review primarily focuses on two key points: (1) miRNAs and their role in human cancer and (2) the regulation of tumor suppressors by miRNAs. The review discusses (a) the regulation of the tumor suppressor p53 by miRNA, (b) the critical role of the miR-144/451 cluster in regulating the Itch-p63-Ago2 pathway, and (c) the regulation of PTEN by miRNAs. Future research and the perspectives of miRNA in cancer are also discussed. Understanding these pathways will open avenues for therapeutic interventions targeting miRNA regulation.

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Section: Mirnas and Cancermentioning

confidence: 99%

How MicroRNAs Command the Battle against Cancer

Wu,

Leng,

Sergi

et al. 2024

IJMS

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“…Moreover, miRNAs powerfully modulate various cellular activities such as cell growth, apoptosis, and differentiation (Saliminejad et al, 2019). It has also been shown that miRNAs play a key role in regulating biological processes and pathways, leading to significant physiological effects (Hwang, Chang, Baek, 2023). In addition, miRNAs exhibit abnormal expression levels in lung cancer and influence its initiation and progression (Li et al, 2022).…”

Section: Effects Of the Microrna-99a-5p/vldlr Axis In Lung Cancer Cel...mentioning

confidence: 99%

Effects of the microRNA-99a-5p/VLDLR axis in lung cancer cell sensitivity to chemotherapy and its mechanism

Lang,

Kong,

Liu

et al. 2023

Braz. J. Pharm. Sci.

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Lung cancer is a major cause of cancer-related death worldwide. This study investigated the regulatory effects of the microRNA-99a-5p (miR-99a-5)/VLDLR axis on lung cancer cell sensitivity to chemotherapy and its mechanism. miR-99a-5p and VLDLR expression levels were quantified using RT-qPCR and western blotting, respectively. The IC50 value of cisplatin (DDP) was determined using a CCK-8 assay. Lung cancer cell proliferation and apoptosis were measured using the CCK-8 assay and flow cytometry, respectively. The mRNA expression levels of apoptosis-related factors (Bax, Bcl-2, and Caspase-3) were evaluated using RT-qPCR. The direct relationship between miR-99a-5p and VLDLR was validated using dual-luciferase reporter gene and RIP assays. miR-99a-5p was weakly expressed in DDP-resistant lung cancer cells. Overexpression of miR-99a-5p promoted DDP sensitivity, suppressed proliferation and colony formation, and promoted apoptosis of A549/DDP cells in vitro. Mechanistically, miR-99a-5p restrained VLDLR expression by binding to VLDLR 3'UTR, and miR-99a-5p mediated inhibition of VLDLR regulated the DDP sensitivity, proliferation, and apoptosis of A549/ DDP cells. Overexpression of miR-99a-5p inhibited the growth of A549 cells and increased chemosensitivity of A549 cells to DDP in vivo. In conclusion, miR-99a-5p overexpression promotes sensitivity to DDP and cell apoptosis by downregulating VLDLR expression in A549/ DDP cells.

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“…Most abundantly expressed small non-coding RNA better known as miRNA plays an important role in cancer progression by targeting subcellular proteins at post-transcriptional or -translational levels (Calin and Croce 2006 ; Hwang et al 2023 ). One of the most interesting features of a miRNA exhibited a context-dependency via regulating multiple targets even in the same cancer types (Genc et al 2023 ).…”

Section: Introductionmentioning

confidence: 99%

MiR-29 and MiR-140 regulate TRAIL-induced drug tolerance in lung cancer

Kim,

Lee,

Yoo

et al. 2024

Animal Cells and Systems

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has chemotherapeutic potential as a regulator of an extrinsic apoptotic ligand, but its effect as a drug is limited by innate and acquired resistance. Recent findings suggest that an intermediate drug tolerance could mediate acquired resistance, which has made the main obstacle for limited utility of TRAIL as an anti-cancer therapeutics. We propose miRNA-dependent epigenetic modification drives the drug tolerant state in TRAIL-induced drug tolerant (TDT). Transcriptomic analysis revealed miR-29 target gene activation in TDT cells, showing oncogenic signature in lung cancer. Also, the restored TRAIL-sensitivity was associated with miR-29ac and 140-5p expressions, which is known as tumor suppressor by suppressing oncogenic protein RSK2 (p90 ribosomal S6 kinase), further confirmed in patient samples. Moreover, we extended this finding into 119 lung cancer cell lines from public data set, suggesting a significant correlation between TRAIL-sensitivity and RSK2 mRNA expression. Finally, we found that increased RSK2 mRNA is responsible for NF-κB activation, which we previously showed as a key determinant in both innate and acquired TRAIL-resistance. Our findings support further investigation of miR-29ac and - 140-5p inhibition to maintain TRAIL-sensitivity and improve the durability of response to TRAIL in lung cancer.

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Determinants of Functional MicroRNA Targeting

Cited by 19 publications

References 158 publications

How MicroRNAs Command the Battle against Cancer

How MicroRNAs Command the Battle against Cancer

Effects of the microRNA-99a-5p/VLDLR axis in lung cancer cell sensitivity to chemotherapy and its mechanism

MiR-29 and MiR-140 regulate TRAIL-induced drug tolerance in lung cancer

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