MiR-329 restricts tumor growth by targeting GRB2 in pancreatic cancer

Wang, Xinjing; Lü, Xiang; Tian, Zhang; Wen, Chenlei; Shi, Minmin; Tang, Xiaomei; Chen, Hao; Peng, Chenghong; Li, Hongwei; Fang, Yuan; Deng, Xiaxing

doi:10.1016/j.pan.2015.12.074

Cited by 12 publications

(15 citation statements)

References 27 publications

(36 reference statements)

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“…What's more, elevated GRB2 expression is associated with cancer progression and poor prognosis . Simultaneously, miR‐411‐5p inhibits the proliferation and metastasis of breast cancer cells by targeting GRB2, whereas miR‐329 limits tumour growth by targeting GRB2 in pancreatic cancer . Through the luciferase reporter assay and Western blotting, we confirmed that GRB2 is the target of miR‐1258.…”

Section: Discussionmentioning

confidence: 58%

MicroRNA‐1258 suppresses tumour progression via GRB2/Ras/Erk pathway in non‐small‐cell lung cancer

et al. 2018

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Section: Discussionmentioning

confidence: 58%

MicroRNA‐1258 suppresses tumour progression via GRB2/Ras/Erk pathway in non‐small‐cell lung cancer

et al. 2018

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“…PDAC cells were cultured in DMEM or RPMI medium supplemented with 10% FBS and 1% penicillin-streptomycin in a humidified chamber at 37 C with 5% CO 2 . Pancreatic patient-derived xenograft (PDX)-derived cancer cells (PDC), including PDC0034, PDC0049, and PDC0001, were isolated from pancreatic PDX tumors and cultured in complete RPMI medium plus 10 ng/mL EGF and 1% ITS as described previously (24). Primary tumor cells from a patient with PDAC samples were directly isolated by Figure 1.…”

Section: Pancreatic Cell Lines and Primary Tumor Cellsmentioning

confidence: 99%

IL22RA1/STAT3 Signaling Promotes Stemness and Tumorigenicity in Pancreatic Cancer

Shi

et al. 2018

Cancer Research

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Chronic inflammation is a feature of pancreatic cancer, but little is known about how immune cells or immune cell-related signals affect pancreatic cancer stemness and development. Our previous work showed that IL22/IL22RA1 plays a vital role in acute and chronic pancreatitis progression by mediating cross-talk between immune cells and acinar cells or stellate cells, respectively. Here, we find IL22RA1 is highly but heterogeneously expressed in pancreatic cancer cells, with high expression associated with poor prognosis of patients with pancreatic cancer. The IL22RA1 population from pancreatic cancer harbored higher stemness potential and tumorigenicity. Notably, IL22 promoted pancreatic cancer stemness via IL22RA1/STAT3 signaling, establishing the mechanism of regulation of cancer stemness by microenvironmental factors. Moreover, STAT3 was indispensable for the maintenance of IL22RA1 cells. Overall, these findings provide a therapeutic strategy for patients with PDAC with high expression of IL22RA1. IL22RA1/STAT3 signaling enhances stemness and tumorigenicity in pancreatic cancer. .

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“…The excess of downregulations is not visible for the hotspot missense mutations; however, it must be noted that due to a very low number of hotspot mutations, the analysis of miRNA levels for this type of mutation is of very low statistical power. Nonetheless, we observed one miRNA, miR-329-3p, playing a role in different cancers [103][104][105][106]), which was consequently downregulated in all three mutational groups. Other downregulated miRNAs playing a role in cancer include (i) miR-1247-5p and miR-1247-3p (in samples with p.S464Ter), recently identified as suppressormiRs [100]; (ii) miR-7-5p (in samples with deleterious mutations), a well-recognized suppressormiR, playing a role in downregulation of the growth, metastasis, and prognosis of various tumors (reviewed in [107]); and (iii) miR-380-5p (in samples with hotspot missense mutations), downregulating TP53 to control cellular survival [108].…”

Section: Functional Consequences Of Smad4 and Smad2 Mutationsmentioning

confidence: 77%

A pan-cancer atlas of somatic mutations in miRNA biogenesis genes

Galka-Marciniak

Urbanek-Trzeciak

Nawrocka

et al. 2020

Preprint

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It is a well-known and intensively studied phenomenon that the levels of many miRNAs are differentiated in cancer. miRNA biogenesis and functional expression are complex processes orchestrated by many proteins cumulatively called miRNA biogenesis proteins. To characterize cancer somatic mutations in the miRNA biogenesis genes and investigate their potential impact on the levels of miRNAs, we analyzed whole-exome sequencing datasets of over 10,000 cancer/normal sample pairs deposited within the TCGA repository. We identified and characterized over 3,600 somatic mutations in 29 miRNA biogenesis genes and showed that some of the genes are overmutated in specific cancers and/or have recurrent hotspot mutations (e.g., SMAD4 in PAAD, COAD, and READ; DICER1 in UCEC; PRKRA in OV; and LIN28B in SKCM). We identified a list of miRNAs whose level is affected by particular types of mutations in either SMAD4, SMAD2, or DICER1 and showed that hotspot mutations in the RNase domains in DICER1 not only decrease the level of 5p-miRNAs but also increase the level of 3p-miRNAs, including many well-known cancer-related miRNAs. We also showed an association of the mutations with patient survival. Eventually, we created an atlas/compendium of miRNA biogenesis alterations providing a useful resource for different aspects of biomedical research.

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MiR-329 restricts tumor growth by targeting GRB2 in pancreatic cancer

Cited by 12 publications

References 27 publications

MicroRNA‐1258 suppresses tumour progression via GRB2/Ras/Erk pathway in non‐small‐cell lung cancer

MicroRNA‐1258 suppresses tumour progression via GRB2/Ras/Erk pathway in non‐small‐cell lung cancer

IL22RA1/STAT3 Signaling Promotes Stemness and Tumorigenicity in Pancreatic Cancer

A pan-cancer atlas of somatic mutations in miRNA biogenesis genes

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