title: FOXC1 promotes melanoma by activating MST1R/PI3K/AKT.
abstract: FOXC1 is a member of Forkhead box family transcription factors. We showed that FOXC1 level was increased in melanoma cells and tissues and correlated with hypomethylation of the FOXC1 gene. Overexpression of FOXC1 promoted proliferation, migration, invasion, colony formation and growth in 3D Matrigel of melanoma cells. FOXC1 increased MST1R and activated the PI3K/AKT pathway. Also, FOXC1 expression was associated with disease progression and poor prognosis of melanoma. We suggest that FOXC1 is a potential prognostic biomarker for treating melanoma and predicting outcome of patients.
authors.affiliation: The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, China.|Department of Molecular Oncology, John Wayne Cancer Institute (JWCI) at Providence Saint John's Health Center, Santa Monica 90404, CA, USA.
authors.forename: Jinhua
authors.initials: J
authors.lastname: Wang
authors.affiliation: The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Endocrinology, Shanxi DAYI Hospital, Shanxi Medical University, Taiyuan, Shanxi 030002, China.
authors.forename: Shiwei
authors.initials: S
authors.lastname: Liu
authors.affiliation: The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.affiliation: The State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing Key Laboratory of Drug Target Research and Drug Screen, Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, China.
authors.forename: Guanhua
authors.initials: G
authors.lastname: Du
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects / Q000235:genetics; D049109:Cell Proliferation / Q000187:drug effects / Q000235:genetics; D051858:Forkhead Transcription Factors / Q000235:genetics* / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D008545:Melanoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D011379:Prognosis; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D034622:RNA Interference; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics; D012878:Skin Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D013449:Sulfonamides / Q000494:pharmacology; D000077484:Vemurafenib
chemical_list: D000970:Antineoplastic Agents; C112743:FOXC1 protein, human; D051858:Forkhead Transcription Factors; D007211:Indoles; D013449:Sulfonamides; D000077484:Vemurafenib; D019869:Phosphatidylinositol 3-Kinases; C080835:RON protein; D020794:Receptor Protein-Tyrosine Kinases; D051057:Proto-Oncogene Proteins c-akt
keywords: FOXC1; MST1R/PI3K/AKT pathway; cutaneous melanoma; methylation