Overexpression of a miR-138–resistant variant of Kindlin-2 overcomes the inhibitory effect of miR-138 on apoptosis and cell spreading induced by loss of.

Slides:

Advertisements

Similar presentations

miR-155 regulates HGAL expression and increases lymphoma cell motility

Advertisements

Interaction of kindlin-2 with integrin β3 promotes outside-in signaling responses by the αVβ3 vitronectin receptor by Zhongji Liao, Hisashi Kato, Manjula.

miR-133a positively regulated p53/p21 pathway.

The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKCθ and ERK pathways by Gilles Despouy, Marjorie Joiner, Emilie Le Toriellec,

Xiang Li, Feng Xu, Ekapun Karoopongse, A

ADAP interactions with talin and kindlin promote platelet integrin αIIbβ3 activation and stable fibrinogen binding by Ana Kasirer-Friede, Jian Kang, Bryan.

Supplementary information

A Previously Unreported Function of β1B Integrin Isoform in Caspase-8-Dependent Integrin-Mediated Keratinocyte Death Roberta Lotti, Alessandra Marconi,

Vascular endothelial growth factor stimulates protein kinase CβII expression in chronic lymphocytic leukemia cells by Simon T. Abrams, Benjamin R. B. Brown,

Volume 141, Issue 2, Pages (August 2011)

Proline supplementation during P5CS protein knockdown suppressed GCN2 activation. Proline supplementation during P5CS protein knockdown suppressed GCN2.

Indomethacin Sensitizes TRAIL-Resistant Melanoma Cells to TRAIL-Induced Apoptosis through ROS-Mediated Upregulation of Death Receptor 5 and Downregulation.

Pioglitazone inhibits aromatase expression in human preadipocytes.

A B CDK2 CDK2 inhibition P Activated KRAS P CP110 CP110

MicroRNA-101 Exerts Tumor-Suppressive Functions in Non-small Cell Lung Cancer through Directly Targeting Enhancer of Zeste Homolog 2 Ji-guang Zhang,

by Silvia Mele, Stephen Devereux, Andrea G

Volume 21, Issue 5, Pages (May 2013)

FOXO3a Is Activated in Response to Hypoxic Stress and Inhibits HIF1-Induced Apoptosis via Regulation of CITED2 Walbert J. Bakker, Isaac S. Harris, Tak.

Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation. Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation.

Interfering with HMGA2 expression blocks transformation in metastatic lung cancer cells. Interfering with HMGA2 expression blocks transformation in metastatic.

Integrin α4β1 and TLR4 Cooperate to Induce Fibrotic Gene Expression in Response to Fibronectin’s EDA Domain Rhiannon M. Kelsh-Lasher, Anthony Ambesi,

Septins Regulate Actin Organization and Cell-Cycle Arrest through Nuclear Accumulation of NCK Mediated by SOCS7 Brandon E. Kremer, Laura A. Adang, Ian.

p38 MAPK activation is required for phosphorylation of Akt at Ser473.

Overexpression of HGF decreases MET protein levels.

Activation of Dual Apoptotic Pathways in Human Melanocytes and Protection by Survivin Tong Liu, Diana Biddle, Adrianne N. Hanks, Brook Brouha, Hui Yan,

Effect of expression of constitutively active CAMKK2 on AMPK activation and the cell cycle in G361 cells. Effect of expression of constitutively active.

Figure 4 DNM1 mutations affect protein levels and self-dimerization (A) HeLa cells were transfected with green fluorescent protein (GFP)-tagged mutant.

Fibronectin-induced integrin-mediated PDGFR-β tyrosine phosphorylation

Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.

Integrin β3 is dispensable for RhoA activity and contractility.

CYP1A1 knockdown increases cell death.

Volume 26, Issue 12, Pages e4 (March 2019)

co-IP of LEDGF/p75 and MeCP2.

Quantification of NMT knockdown.

Targeting eIF4E increases ZEB1 protein and mRNA levels and decreases ZEB1-targeting miR-200c and miR-141 microRNAs. Targeting eIF4E increases ZEB1 protein.

CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.

The role of p53 in H2O2-mediated cell death of hOGG1-deficient H1299 lung carcinoma p53 null cells. The role of p53 in H2O2-mediated cell death of hOGG1-deficient.

Caffeine treatment restores MDM2- and proteasome-dependent degradation of mutant p53 in cancer cells. Caffeine treatment restores MDM2- and proteasome-dependent.

Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells. Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells.

Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. A.

Lamellarin D induces cell death through a Fas-independent pathway.

Lamellarin D activates the intrinsic pathway of apoptosis.

Sensor siRNAs can be used in high-order combinations.

Depletion of HDAC2 sensitizes cells to epirubicin-induced apoptosis.

Clathrin-dependent, constitutive endocytosis of DR4 and DR5 in TRAIL-resistant cells. Clathrin-dependent, constitutive endocytosis of DR4 and DR5 in TRAIL-resistant.

CXCR4 expression levels of MDA-MB-231 cells at 48 hours posttransfection of CXCR4 siRNAs. CXCR4 expression levels of MDA-MB-231 cells at 48 hours posttransfection.

KPT-9274 shows specificity for attenuation of PAK4 targets preferentially in RCC cells. KPT-9274 shows specificity for attenuation of PAK4 targets preferentially.

Volume 23, Issue 4, Pages (April 2015)

Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,

Fig. 3. KMS99220 inhibits activation of NFκB signaling via HO-1 induction. (A) BV2 cells were treated with 10 µM KMS99220 for 1 h, and then treated with.

The effects of HDAC2 knockdown on cell-cycle proteins.

Platinum-based chemotherapy increased TXNIP expression, and overexpression of TXNIP enhanced the effectiveness of this therapy. Platinum-based chemotherapy.

A24 induces apoptosis of MCL cells.

RUNX3 depletion induces cellular senescence and inflammatory cytokine expression in cells undergoing TGFβ-mediated EMT. A, Cells were transfected with.

The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.

Adhesion to fibronectin protects Mcl-1 knockdown cells from apoptosis.

Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. A,

AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.

SAHA blocks IR-induced increase of RAD51 protein in MM cells.

The interaction of PALB2 with BRCA1 is required for the assembly of PALB2, BRCA2, and RAD51 nuclear foci. The interaction of PALB2 with BRCA1 is required.

Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization in 231BR3 cells. Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization.

AXL overexpression decreases proliferation in vitro.

Effect of MIF siRNA on the production of MMP-13 induced by LPA

W. chinensis extract induces apoptosis in AR-dependent prostate cancer cells. W. chinensis extract induces apoptosis in AR-dependent prostate cancer cells.

RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis in ovarian cancer cells. RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis.

Effect of BCAA on the progression of cell cycle, expression of p21CIP1, and induction of apoptosis in HepG2 cells in the presence and absence of visfatin.

Knockdown of NR4A1 induces endoplasmic reticulum stress–mediated apoptosis by increasing ROS production in pancreatic cancer cells. Knockdown of NR4A1.

KDM4A levels affect the distribution of translation initiation factors

Effect of 6-SHO on mouse prostate cancer HMVP2 cells.

Sp1 complementation assay.

Presentation transcript:

Overexpression of a miR-138–resistant variant of Kindlin-2 overcomes the inhibitory effect of miR-138 on apoptosis and cell spreading induced by loss of Kindlin-2 and docetaxel treatment. Overexpression of a miR-138–resistant variant of Kindlin-2 overcomes the inhibitory effect of miR-138 on apoptosis and cell spreading induced by loss of Kindlin-2 and docetaxel treatment. A, Western blots with anti–Kindlin-2 antibody (top) and anti-GFP antibody (middle) of cell lysates from PC3 cells with the indicated transfections. β-Actin served as a loading control. B, representative histograms using flow cytometry of PC3 cells with the indicated transfections after docetaxel treatment and staining with Annexin V for apoptosis. Numbers in parenthesis represent the % change in apoptosis compared to the untreated cells. C, quantification of apoptosis in PC3 cells. Data are the fold-change in cell apoptosis normalized to the values of control cells transfected with GFP and the nontargeting siRNA (GFP/NT) cells. Data are representative of three independent experiments (*, P < 0.05; Student t test). D, representative micrographs of Alexa Fluor 568 phalloidin-stained PC3 cells with the indicated transfections and seeded onto coverslips coated with fibronectin (20 μg/mL) for 2 hours in the presence or absence of docetaxel. E, quantification of PC3 cell spreading under the indicated treatments. Data are the fold-change in cell spreading normalized to the values of untreated cells transfected with GFP and the nontargeting siRNA (GFP/NT). Data are representative of three independent experiments (*, P < 0.05; Student t test). F, schematic diagram illustrating the cross-talk between miR-138, Kindlin-2, and β1-Integrin to dictate the modulation of response to chemotherapeutics. Khalid Sossey-Alaoui, and Edward F. Plow Mol Cancer Res 2016;14:228-238 ©2016 by American Association for Cancer Research