BAD overexpression inhibits cell growth and induces apoptosis via mitochondrial-dependent pathway in non-small cell lung cancer

[1]  Wei-min Li,et al.  Overexpression of Bcl-2-associated death inhibits A549 cell growth in vitro and in vivo. , 2012, Cancer biotherapy & radiopharmaceuticals.

[2]  Wei-min Li,et al.  Loss of Bad expression confers poor prognosis in non-small cell lung cancer , 2012, Medical Oncology.

[3]  J. Wimalasena,et al.  P1-02-11: The BCL2 Antagonist of Death, BAD Is Down-Regulated in Breast Cancer and Inhibits Cancer Cell Invasion. , 2011 .

[4]  Wei-min Li,et al.  Down-regulation of JAK1 by RNA interference inhibits growth of the lung cancer cell line A549 and interferes with the PI3K/mTOR pathway , 2011, Journal of Cancer Research and Clinical Oncology.

[5]  S. Eschrich,et al.  BAD Phosphorylation Determines Ovarian Cancer Chemosensitivity and Patient Survival , 2011, Clinical Cancer Research.

[6]  Wei-min Li,et al.  Activation of mammalian target of rapamycin pathway confers adverse outcome in nonsmall cell lung carcinoma , 2011, Cancer.

[7]  Clare Stirzaker,et al.  Loss of Special AT-Rich Binding Protein 1 Expression is a Marker of Poor Survival in Lung Cancer , 2011, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[8]  U. Rapp,et al.  BAD Contributes to RAF-mediated Proliferation and Cooperates with B-RAF-V600E in Cancer Signaling* , 2011, The Journal of Biological Chemistry.

[9]  D. Ray,et al.  Glucocorticoid receptor over-expression promotes human small cell lung cancer apoptosis in vivo and thereby slows tumor growth , 2010, Endocrine-related cancer.

[10]  L. Tanoue.  Cancer Statistics, 2009 , 2010 .

[11]  H. Ithnin,et al.  Immunohistochemical Detection of Phospho-Akt, Phospho-BAD, HER2 and Oestrogen Receptors α and β in Malaysian Breast Cancer Patients , 2010, Pathology & Oncology Research.

[12]  M. Taniwaki,et al.  Involvement of BH3-only proteins in hematologic malignancies. , 2009, Critical reviews in oncology/hematology.

[13]  M. Willingham,et al.  Expression of the Bcl-2 Protein BAD Promotes Prostate Cancer Growth , 2009, PloS one.

[14]  B. Brown,et al.  Prognostic significance of Akt, phospho-Akt and BAD expression in primary breast cancer. , 2009, European journal of cancer.

[15]  N. Danial.  BAD: undertaker by night, candyman by day , 2008, Oncogene.

[16]  D. Sargent,et al.  Proapoptotic Bad and Bid Protein Expression Predict Survival in Stages II and III Colon Cancers , 2008, Clinical Cancer Research.

[17]  Sang Gyun Kim,et al.  Enzastaurin, a protein kinase C beta inhibitor, suppresses signaling through the ribosomal S6 kinase and bad pathways and induces apoptosis in human gastric cancer cells. , 2008, Cancer research.

[18]  S. Cory,et al.  The Bcl-2 apoptotic switch in cancer development and therapy , 2007, Oncogene.

[19]  Shivendra V. Singh,et al.  Diallyl trisulfide, a constituent of processed garlic, inactivates Akt to trigger mitochondrial translocation of BAD and caspase-mediated apoptosis in human prostate cancer cells. , 2006, Carcinogenesis.

[20]  S. R. Datta,et al.  Bad-deficient mice develop diffuse large B cell lymphoma , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[21]  H. Harada,et al.  Overexpression of BAD potentiates sensitivity to tumor necrosis factor-related apoptosis-inducing ligand treatment in the prostatic carcinoma cell line LNCaP. , 2003, Molecular cancer research : MCR.

[22]  S. Korsmeyer,et al.  Activation of BAD by Therapeutic Inhibition of Epidermal Growth Factor Receptor and Transactivation by Insulin-like Growth Factor Receptor* , 2002, The Journal of Biological Chemistry.

[23]  S. Korsmeyer,et al.  BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. , 2001, Molecular cell.

[24]  P. Vogt,et al.  The growth-promoting activity of the Bad protein in chicken embryo fibroblasts requires binding to protein 14-3-3 , 2001, Oncogene.

[25]  E. Yang,et al.  BAD/BCL-xL heterodimerization leads to bypass of G0/G1 arrest , 2001, Oncogene.

[26]  S. Korsmeyer,et al.  Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death , 2001, Science.

[27]  M. Hengartner.  The biochemistry of apoptosis , 2000, Nature.

[28]  J. Downward.  How BAD phosphorylation is good for survival , 1999, Nature Cell Biology.

[29]  D. Kioussis,et al.  Bad Can Act as a Key Regulator of  T Cell Apoptosis and T Cell Development , 1999, The Journal of experimental medicine.

[30]  D. Kufe,et al.  Cytochrome c-dependent and -independent Induction of Apoptosis in Multiple Myeloma Cells* , 1997, The Journal of Biological Chemistry.

[31]  S. Korsmeyer,et al.  Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell death , 1995, Cell.