The let-7 microRNA reduces tumor growth in mouse models of lung cancer

By A. Esquela-Kerscher, Phong Trang, J. Wiggins, Lubna Patrawala, Angie Cheng, L. Ford, J. Weidhaas, D. Brown, A. Bader, Frank J. Slack. Cell Cycle, 2008

671 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/35f4433c26be273110275d52ff0d7938309fb22d

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Citations in the corpus

MicroRNAs en route to the clinic: progress in validating and targeting microRNAs for cancer therapy (2011, neutral): “Although the initial proof-of-principle studies using miRNAs as therapeutics took advantage of adenoviral-base”
Causes and consequences of microRNA dysregulation in cancer (2009, background): “, are differentially expressed in different tissues and are involved in different human tumour”
A SNP in a let-7 microRNA complementary site in the KRAS 3′UTR Increases Non-Small Cell Lung Cancer Risk (2008, background): “12, 13); their lower levels are biomarkers of a poor outcome (14, 15); they regulate multiple important lung cancer oncogenes, including RAS (12, 16); and they inhibit growth of lung cancer cell lines in vitro (12, 14) and in vivo (17, 18).”
MicroRNA dysregulation in cancer: diagnostics, monitoring and therapeutics. A comprehensive review (2012, neutral): “Using a conditional mouse lung cancer model, where conditional expression of oncogenic K-ras could be activated, Esquela-Kerscher et al showed that the intranasal administration of an adenovirus expressing let-7a RNA hairpin reduced tumour formation in vivo (Esquela-Kerscher et al, 2008).”
MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “Recently, it was shown that let-7 effectively suppresses cancer development in a mouse model of spontaneous lung cancer (Esquela-Kerscher et al., 2008; Kumar et al., 2008), giving hope that it could be useful for cancer therapy.”
Therapeutic delivery of miR-26a inhibits cancer cell proliferation and induces tumor-specific apoptosis (2009, positive): “Supporting this notion, two recent reports demonstrated that viral delivery of let-7 miRNAs suppressed tumor growth in a mouse model of lung adenocarcinoma (Esquela-Kerscher et al., 2008; Kumar et al., 2008).”
Development of a lung cancer therapeutic based on the tumor suppressor microRNA-34 (2010, methodology): “Transfection and proliferation assays were carried out as described (18, 19), and proliferation was assessed using Alamar Blue (Invitrogen) 3 to 7 days after transfection depending on the growth rates of individual cell lines.”
MicroRNAs in development and disease. (2011, background): “It also suppresses growth of tumor xenografts (166, 323) and primary tumors in a K-Ras lung cancer model in vivo, when delivered intranasally via a lentivirus vector (166).”
miR-34 – a microRNA replacement therapy is headed to the clinic (2012, background): “A common approach to achieve miRNA expression in vivo is based on vectoral systems that function similarly to those used for traditional gene therapy (Esquela-Kerscher et al., 2008; Kumar et al., 2008; Kota et al., 2009; Qiu et al., 2011).”
Oncogenic Lin28A and Lin28B inhibit let-7 microRNA biogenesis by distinct mechanisms (2011, neutral): “Restoration of let-7 expression effectively inhibits cancer growth in mouse models of lung and breast cancers (Barh et al., 2010; Esquela-Kerscher et al., 2008; Slack, 2009; Trang et al., 2010; Yu et al., 2007a).”