MicroRNA-21 is an antiapoptotic factor in human glioblastoma cells.

By J. Chan, Anna M. Krichevsky, Kenneth S. Kosik. Cancer Research, 2005

2,600 citations recorded by the source corpus.

MicroRNAs (miRNAs) are small noncoding RNA molecules that regulate protein expression by targeting the mRNA of protein-coding genes for either cleavage or repression of translation. The roles of miRNAs in lineage determination and proliferation as well as the location of several miRNA genes at sites of translocation breakpoints or deletions has led to the speculation that miRNAs could be important factors in the development or maintenance of the neoplastic state. Here we show that the highly malignant human brain tumor, glioblastoma, strongly over-expresses a specific miRNA, miR-21. Our studies show markedly elevated miR-21 levels in human glioblastoma tumor tissues, early-passage glioblastoma cultures, and in six established glioblastoma cell lines (A172, U87, U373, LN229, LN428, and LN308) compared with nonneoplastic fetal and adult brain tissues and compared with cultured nonneoplastic glial cells. Knockdown of miR-21 in cultured glioblastoma cells triggers activation of caspases and leads to increased apoptotic cell death. Our data suggest that aberrantly expressed miR-21 may contribute to the malignant phenotype by blocking expression of critical apoptosis-related genes.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8de8119e007331a5b9e11c3ef99e15b2c7c8edce

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Citations in the corpus

MicroRNA-21 targets a network of key tumor-suppressive pathways in glioblastoma cells. (2008, background): “High levels of miR-21 were first reported in glioblastoma tumors and cell lines (6).”
The neuronal microRNA system (2006, background): “For example, miRNAs involved in malignant transformation target apoptosi”
MicroRNA 21 Promotes Glioma Invasion by Targeting Matrix Metalloproteinase Regulators (2008, methodology): “Since, as demonstrated earlier, the endogenous miR-21 is high in gliomas and many other cancer cell types (5, 54), we hypothesized that its overexpression might have additional regulatory effects on miR-21 targets.”
MicroRNA-21 (miR-21) post-transcriptionally downregulates tumor suppressor Pdcd4 and stimulates invasion, intravasation and metastasis in colorectal cancer (2008, background): “, 2006), antiapoptosis (Chan et al., 2005) and response to gemcitabine-based chemotherapy (Meng et al.”
RNAi therapeutics: principles, prospects and challenges. (2007, background): “MicroRNAs are known to be important regulators of cell differentiation and may function as oncogenes [47] or tumor suppressors [48,49].”
The detection of differentially expressed microRNAs from the serum of ovarian cancer patients using a novel real-time PCR platform. (2009, background): “Among the 5 over-expressed miRNAs that we discovered are three potential oncomirs; mirs-21, 92 and 93. Over-expression of mir-21 has been demonstrated in glioblastoma, breast, colon, prostate, lung, pancreas and stomach cancers [19, 20 ].”
MicroRNAs in Common Human Diseases (2012, background): “In contrast, miR-21 directly serves as an anti-apoptotic factor in glioblastomas and breast cancer [46,51].”
MicroRNA-21 promotes cell transformation by targeting the programmed cell death 4 gene (2008, background): “Recent reports have identified miR-21 as the only miRNA that is overexpressed in nine types of solid tumors (lung, breast, stomach, prostate, colon, brain, head and neck, esophagus and pancreas) (Chan et al., 2005; Iorio et al., 2005; Diederichs and Haber, 2006; Roldo et al., 2006; Volinia et al., 2”
Targeting MicroRNAs in Cancer: Rationale, Strategies and Challenges (2010, neutral): “Chan and colleagues blocked miR-21 expression in glioblastoma cell lines and reported an increased activation of caspases and of apoptosi”