[1] Liu J, FukunagaKalabis M, Li L, et al. Developmental pathways activated in melanocytes and melanoma[J]. Arch Biochem Biophys, 2014, 563: 13-21. DOI: 10.1016/j.abb.2014.07.023.
[2] Yuan X, Wu H, Xu H, et al. Notch signaling: an emerging therapeutic target for cancer treatment[J]. Cancer Lett, 2015, 369(1): 20-27. DOI: 10.1016/j.canlet.2015.07.048.
[3] Bedogni B. Notch signaling in melanoma: interacting pathways and stromal influences that enhance Notch targeting[J]. Pigment Cell Melanoma Res, 2014, 27(2): 162-168. DOI: 10.1111/pcmr.12194.
[4] Zhang JX, Han YP, Bai C, et al. Notch1/3 and p53/p21 are a potential therapeutic target for APSinduced apoptosis in nonsmall cell lung carcinoma cell lines[J]. Int J Clin Exp Med, 2015, 8(8): 12539-12547.
[5] Kang S, Xie J, Miao J, et al. A knockdown of Maml1 that results in melanoma cell senescence promotes an innate and adaptive immune response[J]. Cancer Immunol Immunother, 2013, 62(1): 183-190. DOI: 10.1007/s00262-012-1318-1.
[6] Asnaghi L, Lin MH, Lim KS, et al. Hypoxia promotes uveal melanoma invasion through enhanced Notch and MAPK activation[J]. PLoS One, 2014, 9(8): e105372. DOI: 10.1371/journal.pone.0105372.
[7] Zheng X, Narayanan S, Zheng X, et al. A Notchindependent mechanism contributes to the induction of Hes1 gene expression in response to hypoxia in P19 cells[J]. Exp Cell Res, 2017, 358(2): 129139. DOI: 10.1016/j.yexcr.2017.06.006.
[8] Ishida T, Hijioka H, Kume K, et al. Notch signaling induces EMT in OSCC cell lines in a hypoxic environment[J]. Oncol Lett, 2013, 6(5): 1201-1206. DOI: 10.3892/ol.2013.1549
[9] Moriyama H, Moriyama M, Isshi H, et al. Role of Notch signaling in the maintenance of human mesenchymal stem cellsunder hypoxic conditions[J]. Stem Cells Dev, 2014, 23(18): 2211-2224. DOI: 10.1089/scd.2013.0642.
[10] Zhang K, Wong P, Duan J, et al. An ERBB3/ERBB2 oncogenic unit plays a key role in NRG1 signaling and melanoma cell growth and survival[J]. Pigment Cell Melanoma Res, 2013, 26(3): 408-414. DOI: 10.1111/pcmr.12089.
[11] Zhang K, Wong P, Salvaggio C, et al. Synchronized targeting of Notch and ERBB signaling suppresses melanoma tumor growth through inhibition of Notch1 and ERBB3[J]. J Invest Dermatol, 2016, 136(2): 464472. DOI: 10.1016/j.jid.2015.11.006.
[12] Krepler C, Xiao M, Samanta M, et al. Targeting Notch enhances the efficacy of ERK inhibitors in BRAFV600E melanoma[J]. Oncotarget, 2016, 7(44): 71211-71222. DOI: 10.18632/oncotarget.12078.
[13] Abel EV, Basile KJ, Kugel CH 3rd, et al. Melanoma adapts to RAF/MEK inhibitors through FOXD3mediated upregulation of ERBB3[J]. J Clin Invest, 2013, 123(5): 2155-2168. DOI: 10.1172/JCI65780.
[14] Skarmoutsou E, Bevelacqua V, D′Amico F, et al. FOXP3 expression is modulated by TGF β1/NOTCH1 pathway in human melanoma[J]. Int J Mol Med, 2018, 42(1): 392-404. DOI: 10.3892/ijmm.2018.3618.
[15] Murtas D, Piras F, Minerba L, et al. Activated Notch1 expression is associated with angiogenesis in cutaneous melanoma[J]. Clin Exp Med, 2014, 15(3): 351-360. DOI: 10.1007/s102380140300y.
[16] Liu Y, Su C, Shan Y, et al. Targeting Notch1 inhibits invasion and angiogenesis of human breast cancer cells via inhibition nuclear factorκB signaling[J]. Am J Transl Res, 2016, 8(6): 26812692.
[17] Abbas OL, Borman H, Terzi YK, et al. The Notch pathway is a critical regulator of angiogenesis in a skin model of ischemia[J]. Vasc Med, 2015, 20(3): 205-211. DOI: 10.1177/1358863X15570723.
[18] Ubezio B, Blanco RA, Geudens I, et al. Synchronization of endothelial Dll4Notch dynamics switch blood vessels from branching to expansion[J]. Elife, 2016, 5: pii: e12167. DOI: 10.7554/eLife.12167.
[19] Pitulescu ME, Schmidt I, Giaimo BD, et al. Dll4 and Notch signalling couples sprouting angiogenesis and artery formation[J]. Nat Cell Biol, 2017, 19(8): 915-927. DOI: 10.1038/ncb3555.
[20] Murata A, Hayashi S. Notchmediated cell adhesion[J]. Biology (Basel), 2016, 5(1): pii: E5. DOI: 10.3390/biology5010005.
[21] Zhang JP, Li N, Bai WZ, et al. Notch ligand Deltalike 1 promotes the metastasis of melanoma by enhancing tumor adhesion[J]. Braz J Med Biol Res, 2014, 47(4): 299-306.
[22] Murtas D, Maxia C, Diana A, et al. Role of epithelialmesenchymal transition involved molecules in the progression of cutaneous melanoma[J]. Histochem Cell Biol, 2017, 148(6): 639649. DOI: 10.1007/s0041801716060.
[23] Singh M, Yelle N, Venugopal C, et al. EMT: mechanisms and therapeutic implications[J]. Pharmacol Ther, 2018, 182: 8094. DOI: 10.1016/j.pharmthera.2017.08.009.
[24] Breier G, Grosser M, Rezaei M. Endothelial cadherins in cancer[J]. Cell Tissue Res, 2014, 355(3): 523-527. DOI: 10.1007/s00441-014-1851-7.
[25] LadeKeller J, RiberHansen R, Guldberg P, et al. E to Ncadherin switch in melanoma is associated with decreased expression of phosphatase and tensin homolog and cancer progression[J]. Br J Dermatol, 2013, 169(3): 618-628. DOI: 10.1111/bjd.12426.
[26] Wieland E, RodriguezVita J, Liebler SS, et al. Endothelial Notch1 activity facilitates metastasis[J]. Cancer Cell, 2017, 31(3): 355367. DOI: 10.1016/j.ccell.2017.01.007.
[27] Pearlman RL, Montes de Oca MK, Pal HC, et al. Potential therapeutic targets of epithelialmesenchymal transition in melanoma[J]. Cancer Lett, 2017, 391: 125140. DOI: 10.1016/j.canlet.2017.01.029.
[28] Yuan X, Wu H, Han N, et al. Notch signaling and EMT in nonsmall cell lung cancer: biological significance and therapeutic application[J]. J Hematol Oncol, 2014, 7: 87. DOI: 10.1186/s13045-014-0087-z.
[29] Lin X, Sun B, Zhu D, et al. Notch4+ cancer stemlike cells promote the metastatic and invasive ability of melanoma[J]. Cancer Sci, 2016, 107(8): 1079-1091. DOI: 10.1111/cas.12978.
[30] Golan T, Messer AR, AmitaiLange A, et al. Interactions of melanoma cells with distal keratinocytes krigger metastasis via Notch signaling inhibition of MITF[J]. Mol Cell, 2015, 59(4): 664-676. DOI: 10.1016/j.molcel.2015.06.028. |