miR-765 Acts as a Tumor Promoter and Indicates Poor Prognosis in Non-Small Cell Lung Cancer

Wang, Jiying; Wang, Li; Zhang, Congjun

doi:10.2147/ott.s284212

Cited by 9 publications

(6 citation statements)

References 30 publications

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“…All antimiRs chosen had high to moderate levels of miRNA expression in the selected cell lines. 33 , 39 − 41 In accordance with expectation, we found that antiup-miRs downregulated and antidown-miRs upregulated protein expression for ST6GAL1. For antiup-miRs, a concomitant loss of α-2,6-sialic acid was also observed, supporting a function for these miRNAs in maintenance of sialyltransferase and sialylation levels.…”

Section: Resultssupporting

confidence: 90%

“…To test whether our miRFluR assay is representative of regulation for the actual enzyme ST6GAL1, we validated our findings for a subset of hits (four down-miRs, eight up-miRs). As upregulation was a surprising finding, we validated twice the number of up-miRs and prioritized miRNA with known roles in the literature. − To ensure that our findings were reproducible across cell types, we tested four cancer cell lines: A549 (lung, Figure and Supporting Information Figures S3–S4), PANC1 (pancreatic, Supporting Information Figures S5–S6), HT-29 (colon, Supporting Information Figure S7a–d), and OVCAR3 (ovarian, Supporting Information Figure S7e–h). Consistent with previous work, our assay accurately identified regulation of ST6GAL1 by miRNA .…”

Section: Resultsmentioning

confidence: 99%

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High-Throughput Analysis Reveals miRNA Upregulating α-2,6-Sialic Acid through Direct miRNA–mRNA Interactions

Jame-Chenarboo

Macdonald

et al. 2022

ACS Cent. Sci.

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Chemical biology has revealed the importance of sialic acids as a major signal in physiology and disease. The terminal modification α-2,6-sialic acid is controlled by the enzymes ST6GAL1 and ST6GAL2. Dysregulation of this glycan impacts immunological recognition and cancer development. microRNAs (miRNA, miR), noncoding RNAs that downregulate protein expression, are important regulators of glycosylation. Using our recently developed high-throughput fluorescence assay (miRFluR), we comprehensively mapped the miRNA regulatory landscape of α-2,6-sialyltransferases ST6GAL1 and ST6GAL2. We found, contrary to expectations, the majority of miRNAs upregulate ST6GAL1 and α-2,6-sialylation in a variety of cancer cells. In contrast, miRNAs that regulate ST6GAL2 were predominantly downregulatory. Mutational analysis identified direct binding sites in the 3′-untranslated region (UTR) responsible for upregulation, confirming it is a direct effect. The miRNA binding proteins AGO2 and FXR1 were required for upregulation. Our results upend common assumptions surrounding miRNA, arguing that upregulation by these noncoding RNA is common. Indeed, for some proteins, upregulation may be the dominant function of miRNA. Our work also suggests that upregulatory miRNAs enhance overexpression of ST6GAL1 and α-2,6-sialylation, providing another potential pathway to explain the dysregulation observed in cancer and other disease states.

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Section: Resultssupporting

confidence: 90%

Section: Resultsmentioning

confidence: 99%

High-Throughput Analysis Reveals miRNA Upregulating α-2,6-Sialic Acid through Direct miRNA–mRNA Interactions

Jame-Chenarboo

Macdonald

et al. 2022

ACS Cent. Sci.

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“…30 Another group demonstrated significant upregulation of miR-765 in non-small cell lung cancer cell lines and tissues, which had a correlation with the TNM stages of patients. 31 In osteosarcoma (OS) tissues, miR-765 was discovered to be upregulated. 32 Moreover, miR-765 stimulated the invasion, migration, and proliferation of OS cells by targeting MTUS1.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA long intergenic non-protein-coding RNA 173 contributes to nasopharyngeal carcinoma progression by regulating microRNA-765/Gremlin 1 pathway

Wang

Jiang

2023

Hum Exp Toxicol

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Background Long intergenic non-protein-coding RNA 173 (LINC00173) executes vital functions in various cancers. Nevertheless, its role and expression in nasopharyngeal carcinoma (NPC) have yet to be investigated. Here, we investigated its effects on the malignancy characteristics of NPC and elucidated the potential molecular mechanism of LINC00173 in NPC progression. Methods Quantitative real-time reverse transcription-PCR (qRT-PCR) and immunoblotting were conducted to estimate the LINC00173, microRNA-765 (miR-765), and Gremlin 1 (GREM1) expressions in NPC cells and tissues. Cell counting kit-8 (CCK8), colony formation, and wound healing experiments were done to evaluate the proliferation, growth, and migration of NPC cells, respectively. The tumorous growth of NPC cells in vivo was assessed through the xenograft tumor experiment. Furthermore, the interactions among miR-765, LINC00173, and GREM1 were investigated through bioinformatics analyses, luciferase reporter and RNA immunoprecipitation chip assays. Results An upregulated LINC00173 expression was found in NPC cell lines and tissues. The functional experiments uncovered that its downregulation repressed NPC cell proliferation, growth, and migration. In addition, LINC00173 knockdown hampered the NPC cells’ tumorous growth in vivo. These effects could partially be reversed by downregulating miR-765. GREM1 is a downstream target of miR-765. GREM1 knockdown could repress the proliferation, growth, and migration of NPC cells. Nonetheless, these anti-tumor effects could be abolished by miR-765 downregulation. Mechanistically, LINC00173 increased the expression of GREM1 by binding with miR-765. Conclusions LINC00173 functions as an oncogenic factor by binding with miR-765 to promote the progression of NPC via GREM1 upregulation. This study provides a novel insight into the molecular mechanisms involved in NPC progression.

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“…miR-765 was predicted as a potential target of USP30-AS1, and the function of miR-765 has been demonstrated in numerous human cancers. The upregulation of miR-765 in non-small cell lung cancer and esophageal squamous cell carcinoma was indicated to promote disease development and predict patients' poor outcomes [24,25].…”

Section: Discussionmentioning

confidence: 99%

lncRNA USP30-AS1 sponges miR-765 and modulates the progression of colon cancer

Liu

2022

World J Surg Onc

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Background The incidence and mortality of colon cancer is increasing recently. It is necessary to identify effective biomarkers for the progression and prognosis of colon cancer. To assess the potential of lncRNA USP30-AS1 (USP30-AS1) in serving as the biomarker of colon cancer and unearth the underlying mechanism. Methods There were 123 colon cancer patients enrolled. The expression of USP30-AS1 was evaluated with PCR in tissue and cell samples. The clinical significance of USP30-AS1 was assessed with a series of statistical methods, while the CCK8 and Transwell assay were conducted to estimate its biological effect on the colon cancer cellular processes. In mechanism, the interaction of USP30-AS1 with miR-765 was evaluated with the dual-luciferase reporter assay. Results In colon cancer tissues, the USP30-AS1 downregulation and the miR-765 upregulation were observed, and there was a negative correlation between the USP30-AS1 expression level and the miR-765 expression level. The downregulation of USP30-AS1 related to the malignant progression and served as an adverse prognostic indicator of colon cancer. The overexpression of USP30-AS1 dramatically suppressed colon cancer cellular processes, which was alleviated by miR-765. Conclusions USP30-AS1 predicts the malignancy and prognosis of colon cancer patients. USP30-AS1 suppressed the progression of colon cancer through modulating miR-765.

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miR-765 Acts as a Tumor Promoter and Indicates Poor Prognosis in Non-Small Cell Lung Cancer

Cited by 9 publications

References 30 publications

High-Throughput Analysis Reveals miRNA Upregulating α-2,6-Sialic Acid through Direct miRNA–mRNA Interactions

High-Throughput Analysis Reveals miRNA Upregulating α-2,6-Sialic Acid through Direct miRNA–mRNA Interactions

Long noncoding RNA long intergenic non-protein-coding RNA 173 contributes to nasopharyngeal carcinoma progression by regulating microRNA-765/Gremlin 1 pathway

lncRNA USP30-AS1 sponges miR-765 and modulates the progression of colon cancer

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