miR-16 regulates proliferation and invasion of lung cancer cells via the ERK/MAPK signaling pathway by targeted inhibition of MAPK kinase 1 (MEK1)

Chen, TianMing; Xiao, Qin; Wang, Xiaojun; Wang, Zhongqiu; Hu, Jingwen; Zhang, Zhi; Gong, Zhaohui; Chen, Shilin

doi:10.1177/0300060519856505

Cited by 29 publications

(19 citation statements)

References 28 publications

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“… 41 Decreased MIR-16 expression upregulates expression of MEK1 , which in turn promotes cancer cell invasion and proliferation. 42 Overexpression of MIR-16 downregulates the ERK/MAPK pathway by inhibiting MEK1 expression. Consequently, this reduces clone formation and inhibits cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Signature of Immune Cells Post Reovirus Treatment in KRAS Mutated Colorectal Cancer

Fogel¹,

Samouha²,

Goel³

et al. 2021

CMAR

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Purpose Reovirus propagates with high efficiency in KRAS mutated colorectal cancer (CRC). About 45–50% of CRC patients possess a KRAS mutation. Oncolytic reovirus treatment in combination with chemotherapy was tested in patients possessing KRAS mutated metastatic CRC. This study evaluates the biological responses to reovirus treatment by determining the gene expression patterns in RAS-related signaling pathways. Methods Reovirus was administered as a 60-min intravenous infusion for 5 consecutive days every 28 days, at a tissue culture infective dose (TCID 50 ) of 3×10 10 . Peripheral blood mononuclear cells (PBMCs) were isolated from whole-blood pre- and post-reovirus administration at 48 hr, day-8, and day-15. Clariom_D_Human_Assay was used to determine the expression of vital genes compared to pre-reovirus treatment by RNA sequencing. Using exported sample signals, ΔΔCt method was used to analyze the fold changes of genes within seven gene pathways. Significance was calculated by students-two-tail- t- test. Hierarchical clustering dendrogram was constructed by calculating Pearson’s correlation coefficients. Results As compared to the control, SOS1 [48 hr; 2.49X], RRAS [48 hr; 2.24X], PIK3CB [D8, D15; 2.27X, 3.16X], MIR 16–2 [D15; 1.70X], CHORDC1 [48 hr, D15; 1.89X, 4.54X], RTN4 [48 hr; 4.66X], FAM96A [48 hr; 4.54X], NFKB [D8, D15; 19.0X, 1.42X], CASP8 [D8, D15; 2.11X, 1.77X], and CASP9 [D8; 1.45X] are upregulated post-reovirus. NOS3 [D15; 0.61X], SYNE1 [D8, D15; 0.78X, 0.71X], ANGPT1 [D8; 0.62X], VEGFB [48 hr, D8, D15; 0.44X, 0.28X, 0.28X], JUN [D15; 0.69X], and IGF2 [D8; 0.73X] are downregulated post-reovirus. Fold change values were significant [p<0.05]. Conclusion This study highlights reovirus as a novel treatment option for KRAS mutated CRC and showcases its effect on the expression of crucial genes.

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Section: Discussionmentioning

confidence: 99%

Transcriptome Signature of Immune Cells Post Reovirus Treatment in KRAS Mutated Colorectal Cancer

Fogel¹,

Samouha²,

Goel³

et al. 2021

CMAR

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“…miR-16-5p resides on chromosome 13q14, which is generally deleted in B cell chronic lymphocytic leukemia (22). miR-16-5p is also dysregulated in several cancer types, such as gastric cancer, breast cancer and lung cancer (31,48,49). In prostate cancer (PCa), the 13q allele deletion has also been reported, and the frequency of this is associated with tumor progression.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑16‑5p regulates cell survival, cell cycle and apoptosis by targeting AKT3 in prostate cancer cells

Wang

et al. 2020

Oncol Rep

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Prostate cancer (PCa) is a malignancy with the highest morbidity rate in 105 countries worldwide and was a major cause of cancer-associated death in men in 2018. Accumulating evidence suggests that microRNAs (miRNAs/miRs) have important functions in the carcinogenesis of PCa, and may provide novel treatment targets. Previous studies have indicated that miR-16-5p is associated with PCa. However, the relevance and importance of miR-16-5p in PCa carcinogenesis are still not completely understood. In the current study, we aimed to investigate the role and mechanism of miR-16-5p in PCa carcinogenesis. The results showed that miR-16-5p was markedly downregulated in PCa cells, and MTS assay, colony formation, flow cytometric analyses demonstrated that miR-16-5p inhibited PCa cell survival, regulated cell cycle distribution and induced apoptosis. Moreover, luciferase reporter assay and western blot analysis showed that miR-16-5p directly targets AKT3 (AKT serine/threonine kinase 3), which is associated with PCa carcinogenesis, and the effects of the downregulation of AKT3 were similar to the effects of upregulation of miR-16-5p in PC-3 cells. In conclusion, our data clarify that miR-16-5p has anticancer functions in PCa cells, and our findings provide experimental evidence to highlight the potential value of miR-targeting treatment strategies for PCa.

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“…Subsequently, we examined the abundance of four selected differentially expressed miRNAs (miR-16, miR-181a-3p, miR-223, miR-451) by real-time qPCR in the liver of silver carp exposed for 1, 3, 6, and 12 h to MC-LR (50 and 200 µg/kg); miR-16 was found to act as a tumor suppressor associated with the development of chronic lymphocytic leukemia, breast cancer, lung cancer, and colorectal cancer [46,47]. Accumulated evidence has shown that the expression of miR-16 is decreased in multiple cancer cells, and elevated expression of miR-16 significantly inhibits the proliferation of cancer cells and induces G0/G1 cell cycle arrest [48]. miR-181a plays a key role in the immune response by regulating T cells [49,50].…”

Section: Discussionmentioning

confidence: 99%

Aberrant Expressional Profiling of Known MicroRNAs in the Liver of Silver Carp (Hypophthalmichthys molitrix) Following Microcystin-LR Exposure Based on samllRNA Sequencing

Feng

Chen

et al. 2020

Toxins

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Microcystin-LR (MC-LR) poses a serious threat to human health due to its hepatotoxicity. However, the specific molecular mechanism of miRNAs in MC-LR-induced liver injury has not been determined. The aim of the present study was to determine whether miRNAs are regulated in MC-LR-induced liver toxicity by using high-throughput sequencing. Our research demonstrated that 53 miRNAs and 319 miRNAs were significantly changed after 24 h of treatment with MC-LR (50 and 200 μg/kg, respectively) compared with the control group. GO enrichment analysis revealed that these target genes were related to cellular, metabolic, and single-organism processes. Furthermore, KEGG pathway analysis demonstrated that the target genes of differentially expressed miRNAs in fish liver were primarily involved in the insulin signaling pathway, PPAR signaling pathway, Wnt signaling pathway, and transcriptional misregulation in cancer. Moreover, we hypothesized that 4 miRNAs (miR-16, miR-181a-3p, miR-451, and miR-223) might also participate in MC-LR-induced toxicity in multiple organs of the fish and play regulatory roles according to the qPCR analysis results. Taken together, our results may help to elucidate the biological function of miRNAs in MC-LR-induced toxicity.

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miR-16 regulates proliferation and invasion of lung cancer cells via the ERK/MAPK signaling pathway by targeted inhibition of MAPK kinase 1 (MEK1)

Cited by 29 publications

References 28 publications

Transcriptome Signature of Immune Cells Post Reovirus Treatment in KRAS Mutated Colorectal Cancer

Transcriptome Signature of Immune Cells Post Reovirus Treatment in KRAS Mutated Colorectal Cancer

MicroRNA‑16‑5p regulates cell survival, cell cycle and apoptosis by targeting AKT3 in prostate cancer cells

Aberrant Expressional Profiling of Known MicroRNAs in the Liver of Silver Carp (Hypophthalmichthys molitrix) Following Microcystin-LR Exposure Based on samllRNA Sequencing

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