lung cancer gene and literature database Home
Cancer metastasis database

Annotation category 5

Literatures

Literature evidence

Links to all GeneRIF Items

407018

PubMed (Gene Name)

Literature evidence

23117485 (MIR27A)

Reduced miR-27a increases tumor sphere formation and colony formation in small cell lung cancer.

23650389 (MIR27A)

miR-27a regulates MET, EGFR, and Sprouty2 in lung cancer.

24966325 (MIR27A)

findings support a lung metastasis-promoting function of the miR-23b/27b/24 cluster of miRNAs, which functions in part through the direct inhibition of PSAP in breast cancer

25128483 (MIR27A)

Results suggest that up-regulation of miR-27a could suppress RKIP expression and in turn contribute to chemoresistance of lung adenocarcinoma cells to cisplatin.

28370334 (MIR27A)

miR-27a contributed to cell proliferation and invasion by inhibiting TGF-beta-induced cell cycle arrest. These results suggest that miR-27a may function as an oncogene by regulating SMAD2 and SMAD4 in lung cancer.

28415619 (MIR27A)

our results indicated that rs895819 was a protective factor for cancer in Caucasians and could increase colorectal cancer risk but decrease breast cancer risk. Moreover, rs6505162 was a protective factor for lung cancer.

30539837 (MIR27A)

Study demonstrated that miR-27a contributes to cancer proliferation, migration, and invasion in cancer stem cells from non-small cell lung cancer - H1650 cell line. miR-27a expression was positively correlated with EGFR in lung cancer cell lines and upregulated EGFR expression and activated AKT and ERK in H1650 and xenograft tumor cells.

31319766 (MIR27A)

our results indicated that microRNA-27a-3p acts as a tumor suppressor in non-small lung cancer via targeting homeobox B8.

32212417 (MIR27A)

Exosome miR-27a-3p secreted from adipocytes targets ICOS to promote antitumor immunity in lung adenocarcinoma.

33501823 (MIR27A)

Radio-sensitizing effects of microRNA-27a elevation in lung cancer cells by inhibiting ZEB1 expression and activating DNA damage repair pathway.