miRNA Profiling in Colorectal Cancer Highlights miR-1 Involvement in MET-Dependent Proliferation

Reid, James F.; Sokolova, Viktorija; Zoni, Eugenio; Lampis, Andrea; Pizzamiglio, Sara; Bertan, Claudia; Zanutto, Susanna; Perrone, Francesco; Camerini, Tiziana; Gallino, G.; Verderio, Paolo; Leo, Ermanno; Pilotti, Silvana; Gariboldi, Manuela

doi:10.1158/1541-7786.mcr-11-0342

Cited by 117 publications

(110 citation statements)

References 28 publications

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“…Several studies have dealt with the effects of different microRNAs in RCC, such as miR-21, but not miR-1. Cell proliferative properties of miR-1 have been investigated in various tumor tissues, such as ovarian, lung, colorectal, prostate, bladder and endometrial cancer, as well as RCC (14,(27)(28)(29)(30)(31)(32).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-1 and MicroRNA-21 Individually Regulate Cellular Growth of Non-malignant and Malignant Renal Cells

Ahrend

Kaul

Ziegler

et al. 2017

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Abstract. Background/Aim: Due to its poor prognosis, it is increasingly necessary to understand the biology of renal cell cancer (RCC). Therefore, we investigated the role of microRNAs miR-1 and miR-21 in the growth of RCC cells compared to that of non-malignant renal cells. Materials and Methods: Four malignant cell lines RCC4, A498) Tumorigenesis gives cells an advantage in survival by an increase of proliferation, angiogenesis, immunomodulation and immortality (1-4). Due to its delayed diagnosis until advanced stages, renal cell cancer (RCC) is known as the deadliest neoplasm of the urinary tract (1, 5). Thus, it is more necessary than ever to understand its tumor biology and explore new targets for further therapeutic approaches and prognostic options (6). Former studies suggested that among others, a misguided microRNA expression pattern may be involved in tumor initiation and progression in RCC (7,8). Among such mechanisms, small regulatory RNAs, so-called microRNAs (miRs), can operate as controllers of different proccesses in tumorigenesis, such as cell migration and differentiation, as well as metastasis and apoptosis (9-11). miR-1 and miR-21 are two of numerous representatives of microRNAs. miR-1, initially found in cardiac muscle cells (12), but also found in various tissues (13-15), was strongly suspected of acting as a tumor suppressor due to its antioncogenic properties (16) in prostate, breast and colorectal cancer (13-15); interestingly, the type of tissue in fact determines the biological behavior of miR-1 (9). Sadly, the current data situation for the expression of miR-1 in RCC leaves much to be desired. For this reason, our study aimed to expand the first findings in order to gain a better understanding of the tumor biology of RCC. Similarly to miR-1, miR-21 was also detected in various malignant tissues, such as prostate and lung cancer and their metastases, pancreatic cancer and colorectal cancer (17-21). However, in contrast to miR-1, miR-21 appears to be an oncomir. There are preliminary investigations, showing miR-21 to appear as an oncomir in the case of RCC (22, 23).The fact that cancer cells have a further survival advantage by extending their chromosomal ends by means of endogenic telomerase, not only raises a problem, but also provides a therapeutic approach in cancer therapy (4).In order to gain deeper insight into these issues, as far as we are aware, we are the first to investigate one non-malignant 625 This article is freely accessible online. *These Authors contributed equally to this study. Materials and MethodsCell culture. Human RCC cell lines Caki-1, 786-O, A498 (all Cell Lines Service, Eppelheim, Germany), and RCC4 (Sigma-Aldrich, München, Germany) and the non-malignant renal cell line RC-124 (Cell Lines Service) were applied in this study. Caki-1 and A498 cells were propagated in minimum essential medium (MEM) supplemented with 79.6 mg/l non-essential amino acids, 2 mM L-glutamine, 1 mM sodium pyruvate, 1% penicillline/streptomycin (P/S), and 10% fetal bovine serum (FBS...

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Section: Discussionmentioning

confidence: 99%

MicroRNA-1 and MicroRNA-21 Individually Regulate Cellular Growth of Non-malignant and Malignant Renal Cells

Ahrend

Kaul

Ziegler

et al. 2017

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“…miR-1 regulates cell proliferation and motility by downregulating c-Met (43). The downregulation of c-Met results in the inhibition of cancer cell proliferation, migration, and also increases apoptosis (44).…”

Section: Discussionmentioning

confidence: 99%

The Novel miR-7515 Decreases the Proliferation and Migration of Human Lung Cancer Cells by Targeting c-Met

Lee

Yoo

et al. 2013

Molecular Cancer Research

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MicroRNAs (miRNA) are small noncoding RNAs that regulate gene expression in human diseases, including lung cancer. miRNAs have oncogenic and nononcogenic functions in lung cancer. In this study, we report the identification of a novel miRNA, miR-7515, from lung cancer cells. The novel miR-7515 was characterized using various predictive programs and experimental methods. miR-7515 was able to forming a stem-loop structure and its sequence was conserved in mammals. The expression level of miR-7515 in lung cancer cells and tissues was profiled using TaqMan miRNA assays. miR-7515 was downregulated in lung cancer compared with normal human lung cells and tissues. The target of miR-7515 was determined using a dual luciferase reporter assay. IntroductionThe first microRNA (miRNA) was discovered in Caenorhabditis elegans, (1, 2) and there are currently more than 1,500 human miRNAs listed in miRBase (http://microrna.sanger.ac.uk/index.shtml; ref. 3). miRNAs are endogenous noncoding RNAs that are 18 to 25 nucleotides (nt) in length and are derived from 60 to 80 nt precursor miRNAs refs. 4,5). The stepwise processing of miRNAs requires the double strand-specific ribonuclease (Drosha), the RNase III enzyme Dicer, and the

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“…Furthermore, re-expression of miR-1 in CRC cell lines causes c-Met-driven decrement in cell proliferation and motility, suggesting that miR-1 can be a feasible candidate for clinical trials of c-Met inhibitors in the therapy of metastatic CRC. 128,129 …”

Section: C-met Targeting By Micrornasmentioning

confidence: 99%

The c-Met receptor: Implication for targeted therapies in colorectal cancer

et al. 2017

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c-Met (mesenchymal-epithelial transition factor) is a tyrosine kinase receptor activated by hepatocyte growth factor and regulates multiple biological processes, such as cell scattering, survival, and proliferation. Aberrant c-Met signaling has been implicated in a variety of cancer types, including colorectal cancer. c-Met is genetically altered through various mechanisms that is associated with colorectal cancer progression and metastasis. Especially, in colorectal cancer, preclinical evidence for the aberrant activation of the c-Met signaling exists. Accordingly, molecular targeting of c-Met receptor could be a promising strategy, in the treatment of colorectal cancer patients. Recently, it was also shown that crosstalk between c-Met and other cell surface receptors attributes to tumorigenesis and development of therapeutic resistance. Characterization of the molecular mechanisms through which c-Met crosstalks with other receptors in favor of tumor formation and progression remains to explore. This review will describe the mechanisms of aberrant c-Met signaling in colorectal cancer and discuss on additional roles for c-Met receptor through crosstalk with other tyrosine kinase receptors and cell surface proteins in colorectal cancer. Novel therapeutic approaches for c-Met pathway targeting will also be discussed.

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miRNA Profiling in Colorectal Cancer Highlights miR-1 Involvement in MET-Dependent Proliferation

Cited by 117 publications

References 28 publications

MicroRNA-1 and MicroRNA-21 Individually Regulate Cellular Growth of Non-malignant and Malignant Renal Cells

MicroRNA-1 and MicroRNA-21 Individually Regulate Cellular Growth of Non-malignant and Malignant Renal Cells

The Novel miR-7515 Decreases the Proliferation and Migration of Human Lung Cancer Cells by Targeting c-Met

The c-Met receptor: Implication for targeted therapies in colorectal cancer

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