OBJECTIVETo investigate the role of extracellular regulated kinase (ERK1/2) pathway in cisplatin-induced apoptosis in human ovarian carcinoma cells.

METHODSCisplatin-induced apoptosis were stained with DAPI and was assessed microscopically in human epithelial adenocarcinoma ovarian cell line SKOV3 cells. ERK activation was determined by Western blotting using an anti-phospho-ERK antibody to detect ERK activity. The effect of PD98059 on ERK activity induced by cisplatin was detected by MTT assay.

RESULTSMarked apoptosis of SKOV3 cells resulted from 48 hours treatment with 20 microg/mL cisplatin. Strong activation of ERK was led to by 15 microg/mL cisplatin. Dose response and time course of cisplatin induced apoptosis in SKOV3 cells. Cisplatin-induced ERK activation occurred at 12 hours and increased to highest induction at 24 hours by Western blotting. The effect of PD 98059 on ERK activity induced by cisplatin at the concentration of 100 micromol/L PD 98059. Statistically significant decreased in cell survival were observed with 100 micromol/L PD 98059 at 15 and 20 microg/mL cisplatin (P < 0.05).

CONCLUSIONSCisplatin activates the ERK signaling pathway in ovarian cancer cell line SKOV3. Inhibition of ERK activity enhances sensitivity to cisplatin cytotoxity in ovarian cancer cell line SKOV3. Evaluation of ERK activity could be useful in predicting which ovarian cancer will response most favorably to cisplatin therapy.

Adenocarcinoma ; enzymology ; pathology ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; Cisplatin ; pharmacology ; Enzyme Activation ; drug effects ; Female ; Flavonoids ; pharmacology ; Humans ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases ; metabolism ; Ovarian Neoplasms ; enzymology ; pathology ; Signal Transduction

OBJECTIVETo investigate the expression of integrin-linked kinase (ILK) in primary prostate cancer and its clinical significance.

METHODSThe expression of ILK was analysed in 50 prostate cancer and 16 benign prostatic hyperplasia samples by immunohistochemical staining.

RESULTSThe positive percentage of ILK was 46.0% (23/50) in primary prostate cancer. The higher the grade and the clinical stage of the tumor, the lower the expression of ILK. The positive percentages of ILK were 9.1% (1/11) in the well differentiated type, 56.4% (22/39) in the moderately and poorly differentiated type (chi2 = 12.28, P < 0.01), 24.0% (6/25) in the well and moderately differentiated type, 68.0% (17/25) in the poorly differentiated type (chi2 = 9.74, P < 0.01), 22.6% (7/31) at the A + B stage and 84.0% (16/19) at the C + D stage (chi2 = 11.8, P < 0.01). But in benign prostatic hyperplasia, it was only 6.2% (1/16), significantly lower than in primary prostate cancer (46.0%) (chi2 = 8.27, P < 0.01).

CONCLUSIONThe abnormal expression of ILK plays an important role in the development of primary prostate cancer, and the detection of ILK may be useful for the judgement of tumor development and prognosis.

Aged ; Aged, 80 and over ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Neoplasm Staging ; Prognosis ; Prostatic Neoplasms ; metabolism ; pathology ; Protein-Serine-Threonine Kinases ; biosynthesis

Background/Aims: Chronic hepatitis C (CHC) patients who failed antiviral therapy are at increased risk for hepatocellular carcinoma (HCC). This study assessed the potential role of metformin and statins, medications for diabetes mellitus (DM) and hyperlipidemia (HLP), in reducing HCC risk among these patients. Methods: We included CHC patients from the T-COACH study who failed antiviral therapy. We tracked the onset of HCC 1.5 years post-therapy by linking to Taiwan’s cancer registry data from 2003 to 2019. We accounted for death and liver transplantation as competing risks and employed Gray’s cumulative incidence and Cox subdistribution hazards models to analyze HCC development. Results: Out of 2,779 patients, 480 (17.3%) developed HCC post-therapy. DM patients not using metformin had a 51% increased risk of HCC compared to non-DM patients, while HLP patients on statins had a 50% reduced risk compared to those without HLP. The 5-year HCC incidence was significantly higher for metformin non-users (16.5%) versus non-DM patients (11.3%; adjusted sub-distribution hazard ratio [aSHR]=1.51; P=0.007) and metformin users (3.1%; aSHR=1.59; P=0.022). Statin use in HLP patients correlated with a lower HCC risk (3.8%) compared to non-HLP patients (12.5%; aSHR=0.50; P<0.001). Notably, the increased HCC risk associated with non-use of metformin was primarily seen in non-cirrhotic patients, whereas statins decreased HCC risk in both cirrhotic and non-cirrhotic patients. Conclusions Metformin and statins may have a chemopreventive effect against HCC in CHC patients who failed antiviral therapy. These results support the need for personalized preventive strategies in managing HCC risk.