A Concise Review of MicroRNA-383: Exploring the Insights of Its Function in Tumorigenesis

Qian, Yi; Xie, Wei; Sun, Weibo; Sun, Weichao; Liao, Yi

doi:10.7150/jca.64846

Cited by 14 publications

(8 citation statements)

References 120 publications

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“…In CRC cells, the enforced expression of miR-383 inhibited cell migration and proliferation by attenuating APRIL expression ( Cui et al, 2018 ). Figure 1 shows some gene targets of miR-383 and their function in cancer cell proliferation, EMT, invasion, and metastasis ( Yi et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-383: A tumor suppressor miRNA in human cancer

Jafarzadeh

Noori

Sarrafzadeh

et al. 2022

Front. Cell Dev. Biol.

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Downregulated expression of anti-tumor miR-383 has been found in many kinds of cancer. MiR-383 family members can directly target the 3′-untranslated region (3′-UTR) of the mRNA of some pro-tumor genes to attenuate several cancer-related processes, including cell proliferation, invasion, migration, angiogenesis, immunosuppression, epithelial-mesenchymal transition, glycolysis, chemoresistance, and the development of cancer stem cells, whilst promoting apoptosis. Functionally, miR-383 operates as a tumor inhibitor miRNA in many types of cancer, including breast cancer, hepatocellular carcinoma, gastric cancer, pancreatic cancer, colorectal cancer, esophageal cancer, lung cancer, head and neck cancer, glioma, medulloblastoma, melanoma, prostate cancer, cervical cancer, oral squamous cell carcinoma, thyroid cancer, and B-cell lymphoma. Both pro-tumor and anti-tumor effects have been attributed to miR-383 in ovarian cancer. However, only the pro-tumor effects of miR-383 were reported in cholangiocarcinoma. The restoration of miR-383 expression could be considered a possible treatment for cancer. This review discusses the anti-tumor effects of miR-383 in human cancers, emphasizing their downstream target genes and potential treatment approaches.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-383: A tumor suppressor miRNA in human cancer

Jafarzadeh

Noori

Sarrafzadeh

et al. 2022

Front. Cell Dev. Biol.

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“…Several reports have demonstrated that miR-383 mediates cellular proliferation via regulating the expression pattern of proliferation-associated genes i.e. Cyclin D1 (Yi et.al, 2022). Cyclin D1 is well known in regulating cell proliferation and has been demonstrated to be over expressed in several cancers (Qie S et.al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Role of miRNA 383 in regulating the mitochondrial machinery and carcinogenesis

Maurya,

Raji,

Kumar

2024

Preprint

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MicroRNAs are a class of small non-coding RNAs, which regulate the expression pattern of various genes in a mechanism similar to RNAi. Along with their importance in normal physiology, microRNAs play crucial role in cancer initiation and progression. Various microRNAs have been reported to be associated with the important hallmarks of the cancer including altered mitochondrial machinery. With our in-silico analysis we found that miR 383 has targets on crucial mitochondrial genes involved in electron transport chain. So, next we checked the role of miR 383 in modulation of the mitochondrial machinery and effect of this alteration in the process of carcinogenesis. The results suggested that miR 383 contribute to carcinogenesis, possibly by modulating the mitochondrial machinery via targeting ND4L and ATP6 genes involved in the complex 1 & 5 of electron transport chain.

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“…Cell proliferation, migration and angiogenesis of glioma-exposed endothelial cells were repressed via miR-383-VEGF/VEGFR2-FAK/Src signaling pathway [33]. On the other hand, a few studies identi ed miR-383 as an oncogene, which was highly expressed in cholangiocarcinoma, renal cell carcinoma, epithelial ovarian cell lines and so on [27]. However, the expression le and biofunction of miR-383 in osteosarcoma remain unknown.…”

Section: Discussionmentioning

confidence: 99%

“…MiR-383 acts as a tumor suppressor and is downregulated in various cancers [22][23][24][25][26]. This miRNA was reported can inhibit tumors from various phenotypes, including proliferation, differentiation, invasion and metastasis [27].…”

Section: Introductionmentioning

confidence: 99%

MiR-383 sensitizes osteosarcoma cells to cisplatin treatment via down-regulating PSMB5

Wang

Bai

Dang

et al. 2023

Preprint

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Background： Proteasome inhibition represents a promising strategy for cancer therapy. Bortezomib, primarily targeting the chymotrypsin-like activity of PSMB5, has been proven effective in several tumors. However, variable sensitivity exits in response to bortezomib, which may be partially due to differences in the expression of proteasome subunits. Methods and Results: In this study, we investigated whether miR-383 affects the proteasome subunits expression in osteosarcoma (OS) cells, and if so, whether OS cells display differential sensitivity to bortezomib concerning miR-383 expression. We detected a decreased miR-383 expression in OS cells and tissues. Then we found a negative correlation between bortezomib cytotoxicity and proteasome 20S core particle subunit β5 (PSMB5) expression level. Intriguingly, we found that PSMB5 is a target of miR-383. Higher expression of miR-383 led to decreased PSMB5 expression and exhibited greater sensitivity to bortezomib in OS cells. Conclusions: In summary, our results represent the first comprehensive analysis of the role of miR-383 in OS. The results suggest that miR-383 may enhance the anticancer effect of bortezomib through PSMB5 repression, providing a novel therapeutic strategy in OS and a new pathway for proteasome regulation.

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A Concise Review of MicroRNA-383: Exploring the Insights of Its Function in Tumorigenesis

Cited by 14 publications

References 120 publications

MicroRNA-383: A tumor suppressor miRNA in human cancer

MicroRNA-383: A tumor suppressor miRNA in human cancer

Role of miRNA 383 in regulating the mitochondrial machinery and carcinogenesis

MiR-383 sensitizes osteosarcoma cells to cisplatin treatment via down-regulating PSMB5

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