Presentation is loading. Please wait.

Presentation is loading. Please wait.

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

Published byHilary McKinney Modified over 5 years ago

Similar presentations

Presentation on theme: "Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,"— Presentation transcript:

1 Per1 inhibits growth and induces apoptosis in prostate cancer cell lines.
Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP, PC3, and DU145 cells were transfected with either empty vector or Per1 expression vector followed by (A) colony formation assay and (B) Annexin V/propidium iodide staining. The percentage of early apoptotic cells is shown. Representative of three independent experiments. Qi Cao et al. Cancer Res 2009;69: ©2009 by American Association for Cancer Research

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

Similar presentations

Inhibition of C13orf19 mRNA expression by siRNA in prostate cancer cells * Introduction A high proportion of bladder cancer.

Inhibition of C13orf19 mRNA expression by siRNA in prostate cancer cells * Introduction A high proportion of bladder cancer.
Discussion The C13orf19 mRNA inhibition by D5 has no effects on cellular growth properties. We suppose that the inhibition leads to reduced apoptosis in.

Discussion The C13orf19 mRNA inhibition by D5 has no effects on cellular growth properties. We suppose that the inhibition leads to reduced apoptosis in.
Figure 5. FK866 caused apoptosis in MCF-7 cells while nicotinamide adenine dinucleotide (NAD+) reversed FK866-induced apoptosis. (A) Representative quadrant.

Figure 5. FK866 caused apoptosis in MCF-7 cells while nicotinamide adenine dinucleotide (NAD+) reversed FK866-induced apoptosis. (A) Representative quadrant.
Fig. 4. Effect of Mcl-1 overexpression on H2O2-induced JNK activation and apoptosis. (A) Expression of Mcl-1 protein in several.

Fig. 4. Effect of Mcl-1 overexpression on H2O2-induced JNK activation and apoptosis. (A) Expression of Mcl-1 protein in several.
Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.

Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.
Full‐length XIAPs that retain caspase 9 inhibitory potential inhibit UV‐induced cell death. Full‐length XIAPs that retain caspase 9 inhibitory potential.

Full‐length XIAPs that retain caspase 9 inhibitory potential inhibit UV‐induced cell death. Full‐length XIAPs that retain caspase 9 inhibitory potential.
NF1 silencing confers resistance of PC9 lung adenocarcinoma cells to erlotinib (erl). NF1 silencing confers resistance of PC9 lung adenocarcinoma cells.

NF1 silencing confers resistance of PC9 lung adenocarcinoma cells to erlotinib (erl). NF1 silencing confers resistance of PC9 lung adenocarcinoma cells.
Supplementary Figure 2. Effect of IL-32 and siRNA of IL-32 on melanoma, colon and prostate cancer cell growth and apoptosis as well as IL-32 expression.

Supplementary Figure 2. Effect of IL-32 and siRNA of IL-32 on melanoma, colon and prostate cancer cell growth and apoptosis as well as IL-32 expression.
Interfering with HMGA2 expression blocks transformation in metastatic lung cancer cells. Interfering with HMGA2 expression blocks transformation in metastatic.

Interfering with HMGA2 expression blocks transformation in metastatic lung cancer cells. Interfering with HMGA2 expression blocks transformation in metastatic.
Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced senescence. Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced.

Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced senescence. Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced.
ROS induction and ATR inhibition synergize in inducing multiple myeloma (MM) cell death. ROS induction and ATR inhibition synergize in inducing multiple.

ROS induction and ATR inhibition synergize in inducing multiple myeloma (MM) cell death. ROS induction and ATR inhibition synergize in inducing multiple.
AKT2, but not AKT1, is required for regulating survival of PTEN-deficient prostate tumor spheroids. AKT2, but not AKT1, is required for regulating survival.

AKT2, but not AKT1, is required for regulating survival of PTEN-deficient prostate tumor spheroids. AKT2, but not AKT1, is required for regulating survival.
Fig. 4 ALRN-6924 inhibits cellular proliferation and clonogenic capacity, and induces cell cycle arrest and apoptosis in AML cell lines. ALRN-6924 inhibits.

Fig. 4 ALRN-6924 inhibits cellular proliferation and clonogenic capacity, and induces cell cycle arrest and apoptosis in AML cell lines. ALRN-6924 inhibits.
USP2a overexpression modifies the microRNA expression profile of prostate cells. USP2a overexpression modifies the microRNA expression profile of prostate.

USP2a overexpression modifies the microRNA expression profile of prostate cells. USP2a overexpression modifies the microRNA expression profile of prostate.
USP2a regulates MYC expression through the MDM2–p53 axis.

USP2a regulates MYC expression through the MDM2–p53 axis.
Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.

Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.
SW fraction induces S phase arrest and apoptosis.

SW fraction induces S phase arrest and apoptosis.
Flow cytometric analysis of apoptotic cells.

Flow cytometric analysis of apoptotic cells.
Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells. Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells.

Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells. Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells.
CYP1A1 knockdown increases cell death.

CYP1A1 knockdown increases cell death.

Similar presentations

Ads by Google