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IL6 — MCL1

Text-mined interactions from Literome

Puthier et al., Br J Haematol 1999 (Multiple Myeloma) : In a system of apoptosis by growth factor deprivation on myeloma cells, we showed that the effect of Bcl-2 seemed minimal whereas Mcl-1 and Bcl-xL were tightly regulated by interleukin (IL)-6
Puthier et al., Eur J Immunol 1999 (MAP Kinase Signaling System...) : In conclusion, our data suggest the involvement of the JAK / STAT pathway but not of the Ras / mitogen activated protein ( MAP ) kinase pathway in IL-6 induced Mcl-1 up-regulation
Kuo et al., Oncogene 2001 : Mcl-1 , but not other Bcl-2 family members, was rapidly up-regulated by IL-6 , with a peak ( approximately 3-4-fold ) appearing at 4 h. Transient transfection of cells with a mcl-1 antisense vector, resulting in a 50-60 % reduction of the anti-apoptotic effect of IL-6, indicating that Mcl-1 is a downstream effector of IL-6 ... Blocking JAK/STAT3 activation with a dominant negative mutant STAT3F or a JAK inhibitor AG490 could not influence IL-6 mediated Mcl-1 up-regulation ... However, the IL-6 induced Mcl-1 up-regulation was effectively attenuated in the presence of PI 3-K inhibitors, LY294002 and wortmannin ... Expression of dominant negative Akt, but not Etk, could abrogate the IL-6 induced increase of Mcl-1 ... In conclusion, our results suggest that the anti-apoptotic effect of IL-6 is mediated , at least in part, by Mcl-1 expression and that is mainly through the PI 3-K/ Akt dependent pathway
Wei et al., Oncogene 2001 (Carcinoma, Squamous Cell...) : This study hypothesizes that the expression of Mcl-1 in cervical cancer cells is regulated by IL-6 ... Blocking the STAT3 or MAPK pathway with dominant negative mutant STAT3F or the MEK inhibitor PD98059 failed to inhibit IL-6 mediated Mcl-1 expression ... Meanwhile, the IL-6 induced Mcl-1 up-regulation was effectively abolished by treatment with PI 3-K inhibitors, LY294002 ... Additionally, overexpression of dominant negative ( dn ) Akt in C33A cells could inhibit the IL-6 induced increase of Mcl-1
Lin et al., Carcinogenesis 2001 (Stomach Neoplasms) : We further found that Mcl-1 , but not other Bcl-2 family members, was up-regulated by IL-6 , by a substantial level over 24 h
Song et al., Chin Med J (Engl) 2002 (Multiple Myeloma) : Mcl-1 , instead of Bcl-2 and Bcl-kappa ( L ), plays an important role in IL-6 deprivation induced apoptosis in XG-7 human myeloma cells
Jee et al., J Invest Dermatol 2002 (Carcinoma, Basal Cell...) : The phosphotidyl inositol 3-kinase/Akt signal pathway is involved in interleukin-6 mediated Mcl-1 upregulation and anti-apoptosis activity in basal cell carcinoma cells ... Use of the two phosphotidyl inositol 3-kinase inhibitors, LY294002 and wortmannin, to check whether this pathway is involved in Mcl-1 upregulation by interleukin-6 , we found that the phosphotidyl inositol 3-kinase inhibitors completely attenuated the interleukin-6 induced Mcl-1 upregulation
Song et al., Chin J Cancer 2002 (Multiple Myeloma) : In addition, up-regulation of Mcl-1 expression induced by IL-6 was significantly inhibited in the presence of AG490, while not of PD98059 and LY294002
Brocke-Heidrich et al., Blood 2004 (Multiple Myeloma) : Among the antiapoptotic members of the B-cell lymphoma-2 (Bcl-2) family of apoptosis regulators, only myeloid cell factor-1 (Mcl-1) was slightly induced by IL-6
Leu et al., Oncogene 2003 (Esophageal Neoplasms) : While Bcl-2, Bcl-x ( L, ), and Bax were not affected, Mcl-1 was induced by IL-6 in human esophageal carcinoma cells
Zhou et al., Int J Hematol 2004 (Multiple Myeloma) : In CD45+ U266 cells, IL-6 increased tyrosine phosphorylation of gp130 and STAT3 and stimulated the level of Mcl-1 protein expression
Kobayashi et al., Gastroenterology 2005 (Cholangiocarcinoma...) : Interleukin-6 contributes to Mcl-1 up-regulation and TRAIL resistance via an Akt signaling pathway in cholangiocarcinoma cells ... The present study evaluated the possibility that IL-6 signaling contributes to Mcl-1 up-regulation in cholangiocarcinoma
Isomoto et al., Hepatology 2005 (Bile Duct Neoplasms...) : We examined this cascade in IL-6 regulation of Mcl-1 transcription in human cholangiocarcinoma cell lines
Meng et al., J Hepatol 2006 (Bile Duct Neoplasms...) : Mcl-1 is identified as a mediator of IL-6 induced tumor cell survival and shown to be transcriptionally regulated by IL-6 via a p38 MAPK dependent pathway
Isomoto et al., Gastroenterology 2007 (Bile Duct Neoplasms...) : Enforced expression of SOCS-3 also reduced IL-6 induction of phospho-STAT-3 and Mcl-1
Li et al., Br J Haematol 2007 (Multiple Myeloma) : IL-6 stimulation or retroviral mediated overexpression of SPHK1 in MM cells resulted in increased intracellular SPHK activity and upregulation of myeloid cell leukaemia-1 (Mcl-1) , leading to increased cell proliferation and survival ... Conversely, inhibition of SPHK1 by small interfering RNA reduced IL-6 induced upregulation of Mcl-1 and blocked the suppressive effect of IL-6 on MM cell apoptosis
Cheng et al., Clin Cancer Res 2008 (Carcinoma, Non-Small-Cell Lung...) : Phosphatidylinositol-3-OH kinase pathway was the major pathway contributing to the up-regulation of Mcl-1 by IL-6 in HPV infected lung cancer cells
Chou et al., Int J Radiat Oncol Biol Phys 2009 : In the presence of sIL6-Ralpha, radiation induced IL-6 expression acts through Mcl-1 expression to rescue endothelial cells from radiation induced death
Chou et al., PloS one 2013 : Serum IL-6 levels were determined by enzyme immunoassays ; signal transduction of IL-6 regulated Mcl-1L expression was verified by chemical inhibitors and decoy double stranded oligodeoxynucleotides ... Chemical inhibition and decoy oligonucleotide competition demonstrated that IL-6 induced Mcl-1L production required signaling mediated by JAK kinase, phosphoinositide 3-kinase (PI3K), and cAMP response-element binding ( CREB ) proteins ... The expression of Mcl-1L is induced by IL-6 through the JAK/PI3K/Akt/CREB signaling pathway
Gruber et al., Cell reports 2013 (Liver Neoplasms, Experimental...) : IL-6 regulates Mcl-1 stability via the inhibition of PP-1a expression, promoting GSK-3ß inactivation