Inhibition of PDCD6 Induces Cell Proliferation and Reduces Apoptosis in Human Epithelial Ovarian Cancer Cells Yan Huang, Xiaohua Wu Department of Gynecology,

Slides:

Advertisements

Similar presentations

The interaction between the Wnt –and Notch-pathways in colorectal cancer development by: John Grünberg The aim is to study the interaction between the.

Advertisements

Abstract Glioblastoma multiforme (GBM) is the most common brain cancer of middle aged Americans. Unfortunately, survival rates are typically less than.

The Story of Bcl-2 Linking cell apoptosis to tumor metastasis Crystal structure of Bcl-2 complex By Yaming Wang.

Maternal and Children Health Care of Shanxi Province

When mammalian cells are subjected to stress signals, oxygen deficiency, radiation, DNA damage, or Chemo- therapeutic drugs, p53 is activated, leading.

Inhibition of SHH signaling enhances Docetaxel efficacy in castration-resistant prostate cancer cells Sierra L. Lawhorne 1,2, Sakthivel Muniyan 1, Parthasarathy.

Signaling Pathways Produced By Combining DsRNA with Paclitaxal to treat Ovarian Cancer Switu Patel.

PDAM is frequently downregulated in oligodendroglial tumors and its knockdown by siRNA induces cisplatin resistance Ng Ho-Keung 吳浩強 The State Key Laboratory.

Apoptosis (Programmed Cell Death). Apoptosis vs Necrosis Level of stress, change in environment stress apoptosisnecrosis.

Livin in Prognosis of Childhood ALL Livin- member of inhibitor of apoptosis proteins (IAP). – IAP- acts on effector and initiator caspases Function of.

Isosteviol derivatives induced apoptosis in Human lung cancer via targeting MEK/MAPK pathway: An in vitro and in vivo study Ahmed M Malki 1,,PhD Stephen.

 Dr. Steven Grant  Dr. Roberto Rosato  Jorge Almenara  Stefanie Coe  Dr. Allison Johnson, HHMI Coordinator.

The Effect of BRCA1 on the Progesterone Receptor.

Relationship Between STAT3 Inhibition and the Presence of p53 on Cyclin D1 Gene Expression in Human Breast Cancer Cell Lines Introduction STAT3 and p53.

Targeting of reactive oxygen species can be a potential therapeutic strategy for cancer treatment Ying-Ray Lee 1, San-Yuan Chen 2, and Hau-Ren Chen 3 1.

第三章 Survivin siRNA nano particles are capable of inhibiting liver cancer cell growth both in vitro and in vivo Suoqin Tang,MD, Kuiyao Qu,MD, Yi Zhang,MD.

Lactate dehydrogenase is crucial for tumor associated macrophage protection of multiple myeloma cells against chemotherapy Carolyn Stierhoff, Enguang Bi,

Cell Physiol Biochem 2014;33: DOI: /

Induction of Forkhead Class box O3a and apoptosis by a standardized ginsenoside formulation, KG-135, is potentiated by autophagy blockade in A549 human.

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2 Cell.

Cell Physiol Biochem 2013;31: DOI: /

Loss of Hdac3 impairs Ar signaling in mouse prostate tissues and has no effect on apoptosis Loss of Hdac3 impairs Ar signaling in mouse prostate tissues.

Rab11-FIP3 silencing upregulates TCR-CD3 cell surface expression in an Lck-dependent manner. Rab11-FIP3 silencing upregulates TCR-CD3 cell surface expression.

Endoplasmic Reticulum Stress Promotes Autophagy and Apoptosis and Reduces Chemotherapy Resistance in Mutant p53 Lung Cancer Cells Cell Physiol Biochem.

miR-133a positively regulated p53/p21 pathway.

by Pascal Gelebart, Mona Anand, Hanan Armanious, Anthea C

Droxinostat, a Histone Deacetylase Inhibitor, Induces Apoptosis in Hepatocellular Carcinoma Cell Lines via Activation of the Mitochondrial Pathway and.

The Chemopreventive Effect of Tanacetum Polycephalum Against LA7-Induced Breast Cancer in Rats and the Apoptotic Effect of a Cytotoxic Sesquiterpene.

Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia by Xue-Fei Huang, Shao-Kai Luo,

MDH2 Stimulated by Estrogen-GPR30 Pathway Down-Regulated PTEN Expression Promoting the Proliferation and Invasion of Cells in Endometrial Cancer Yan.

Activation of ATF4 mediates unwanted Mcl-1 accumulation by proteasome inhibition by Jinsong Hu, Nana Dang, Eline Menu, Elke De Bryune, Dehui Xu, Ben Van.

Pegylated arginase I: a potential therapeutic approach in T-ALL

Fas NF-κB JNK Bcl-2 Akt p21 Bax Ras TRAILR p53 EGFR TRADD Myc TNFR

Mechanisms of apoptosis and growth arrest by isothiocyanates.

A FOXO3a-BIM cascade mediates sensitivity to PARP and MEK inhibition

HPV Type 16 Infection Switches Keratinocytes from Apoptotic to Proliferative Fate under TWEAK/Fn14 Interaction Hong Cheng, Na Zhan, Dong Ding, Xiaoming.

Michèle Algarté-Génin, Olivier Cussenot, Pierre Costa European Urology

Volume 19, Issue 10, Pages (October 2017)

RORα inhibits cell proliferation and expression of the E2F1-targeted genes. RORα inhibits cell proliferation and expression of the E2F1-targeted genes.

Uc.454 Inhibited Growth by Targeting Heat Shock Protein Family A Member 12B in Non- Small-Cell Lung Cancer Jun Zhou, Chenghai Wang, Weijuan Gong, Yandan.

The Human Immunodeficiency Virus Protease Inhibitor Ritonavir Inhibits Lung Cancer Cells, in Part, by Inhibition of Survivin Anjaiah Srirangam, PhD,

A20 inhibits caspase-8 cleavage and TRAIL-induced apoptosis.

Molecular Therapy - Nucleic Acids

ERK1/2 Is Highly Phosphorylated in Melanoma Metastases and Protects Melanoma Cells from Cisplatin-Mediated Apoptosis Alireza Mirmohammadsadegh, Rodrigo.

Figure 1 Extrinsic and intrinsic pathways of apoptosis

Glutamine addiction and cancer invasiveness are positively correlated in ovarian cancer cells (OVCA) Gln deprivation effect on proliferation rate of a.

BAK oligomerization in cells treated by UV is

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

Ectopic expression of caveolin-1 in ZR75 human breast cancer cells downregulated survivin and decreased cell proliferation. Ectopic expression of caveolin-1.

Effect of GSK-3β inhibition on cell-confluence-induced apoptosis.

The effects of the FASN blocker C75 on cell growth and survival (A, E, and F), on expression/phosphorylation of PI3K and MAPK signaling proteins and on.

TSLP and Th2 Cells TSLP TSLP TSLP

Fig. 4. Effects of natriuretic peptide receptor 2 (NPR2) knockdown on cells apoptosis in mouse Leydig cells. (A) Relative mRNA expression of cell apoptosis.

Figure 4. Effects of chloride channel-3 (ClC-3) knockdown on the expression of cell cycle-regulatory proteins. (A) Representative western blot images of.

Representative Western blot analyses of S-phase and other proteins from PC3 cell lysates obtained 3 days after oligomer (400 nm)/Lipofectin (15 μg/ml)

PRIMA-1Met inhibits the growth of multiple myeloma tumors with mutant p53 in vivo. PRIMA-1Met inhibits the growth of multiple myeloma tumors with mutant.

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.

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.

Cisplatin plus PTUPB decreases proliferation and angiogenesis but increases apoptosis as determined by immunohistochemical (IHC) analysis. Cisplatin plus.

ONC201 activates an ISR, decreases cyclin D1 expression, and causes an accumulation of cells in G1 in TNBC cells sensitive to the compounds' antiproliferative.

LY induces cytotoxicity in hMECs via inhibition of Akt/p70S6K kinase activities. LY induces cytotoxicity in hMECs via inhibition of Akt/p70S6K.

PTEN expression regulates autophagy in tumor cells, reducing T cell–mediated killing. PTEN expression regulates autophagy in tumor cells, reducing T cell–mediated.

The effects of HDAC2 knockdown on cell-cycle proteins.

A24 induces apoptosis of MCL cells.

PARP1 suppresses the transcription of PD-L1 in 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.

Blockade of cell cycle at G2-M phase in Bel-7402 cells treated with IG-105. Blockade of cell cycle at G2-M phase in Bel-7402 cells treated with IG-105.

Quercetin induces autophagy, blocks cell cycle and activation of ERK and JNK signaling pathways participates in the G1 arrest in P39 cells. Quercetin induces.

Presentation transcript:

Inhibition of PDCD6 Induces Cell Proliferation and Reduces Apoptosis in Human Epithelial Ovarian Cancer Cells Yan Huang, Xiaohua Wu Department of Gynecology, Cancer Center, Fudan University Yan Huang （310108197903152242） Correspondence: Xiaohua Wu

Backgrounds Ovarian epithelial cancer is the leading killer among all gynecological malignancies. Recent findings suggested that apoptosis and apoptosis-linked genes may play an important role in the development and progression of ovarian cancer (la Cour JM, et al. Mol Oncol. 2008). Programmed cell death gene 6 (PDCD6), also known as apoptosis-linked gene-2 (ALG-2), is a 22 kDa penta-EF-hand type Ca2+-binding protein that was first reported by Vito in 1996. It is well recognized as an apoptotic mediator because PDCD6 expression is required for apoptosis following numerous death stimuli (Vito P, et al. Science. 1996).

Methods BrdU Poliferation Design of siRNA and construction of recombi-nant plasmids RT-PCR, Western blot Flow cytometry Transfection SKOV-3 and OVCAR-3 Apoptosis RT-PCR, Western blot Flow cytometry Cell cycle RT-PCR, Western blot Effects of cisplatin on ovarian cancer cells SKOV-3 and OVCAR-3 BrdU, Flow cytometry Poliferation Apoptosis PDCD6 RT-PCR, Western blot

Results RNAi inhibited PDCD6 expression in ovarian cancer cells

Inhibition of PDCD6 prohibited apoptosis and increased cell proliferation

Inhibition of PDCD6 induced cell cycle Cell cycle phase Transfection group G0/G1(%) S(%) G2/M(%) SKOV-3 control 75.23±1.17 16.87±0.58 7.90±1.39 SKOV-3 pRT-neg 76.73±1.53 15.40±1.21 7.87±1.45 SKOV-3 pRT-pdcd 56.77±1.48a 26.27±1.11a 16.97±2.56a OVCAR-3 control 79.90±1.35 17.17±1.11 2.93±1.08 OVCAR-3 pRT-neg 78.27±1.00 17.30±1.13 4.43±2.05 OVCAR-3 pRT-pdcd 59.27±0.90b 22.17±1.80b 18.57±1.53b

Cisplatin inhibited proliferation and increased apoptosis

PDCD6 RNAi partly blocked the apoptotic effect and the anti-proliferative effect induced by cisplatin

Conclusions 1. Inhibition of PDCD6 by RNAi induced cell proliferation and cell cycle in SKOV-3 and OVCAR-3 cells by up-regulating cyclin D1, cyclin B1, cyclin E, and proliferating cell nuclear antigen (PCNA). 2. Inhibition of PDCD6 by RNAi reduced apoptosis in SKOV-3 and OVCAR-3 cells by decreasing cleaved caspase-3, cleaved caspase-7, cleaved caspase-8, Bax, death receptor 5 (DR5）and death receptor 4(DR4) and increasing Bcl-2.

3. Cisplatin increased cell apoptosis and prohibited cell proliferation while the mRNA and protein expression of PDCD6 was up-regulated. 4. PDCD6 RNAi partly blocked the apoptotic effect and the anti-proliferative effect induced by cisplatin. Cisplatin may inhibit proliferation and increase apoptosis partly through PDCD6. 5. PDCD6 plays an important role in the promotion and progression of ovarian cancer. PDCD6 is a candidate as a new target for ovarian cancer treatment.

Thank you