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1.
Cell Biol Int ; 47(8): 1381-1391, 2023 Aug.
Article in English | MEDLINE | ID: mdl-37067236

ABSTRACT

Cholangiocarcinoma (CCA) is a type of epithelial cancer with poor outcomes and late diagnosis. Accumulating evidence has demonstrated the promoting role of plasminogen activator, urokinase (PLAU) in several tumor types, while its function in CCA is largely unknown. The expression of PLAU in CCA was determined by data from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) database and further confirmed in human tissues using immunohistochemical (IHC) staining. Moreover, PLAU-silencing CCA cell models were constructed for subsequent functional assays in vitro and in vivo. PLAU expression in CCA was significantly higher than that in normal tissues. High PLAU expression was positively correlated with poor patients' survival. PLAU knockdown remarkably suppressed proliferation and migration of CCA cells, whereas enhanced apoptosis. Consistently, tumor growth in mice injected with PLAU-silencing CCA cells was also impaired. Furthermore, we revealed that the activation of NF-κB signaling was required for PLAU-induced malignant phenotypes of CCA cells. Inhibiting the high expression of PLAU in CCA may be a potential entry point for targeted therapy in CCA patient.


Subject(s)
Bile Duct Neoplasms , Cholangiocarcinoma , Humans , Animals , Mice , NF-kappa B/metabolism , Urokinase-Type Plasminogen Activator/metabolism , Plasminogen Activators/metabolism , Signal Transduction , Cholangiocarcinoma/genetics , Cholangiocarcinoma/metabolism , Cholangiocarcinoma/pathology , Bile Ducts, Intrahepatic/metabolism , Bile Ducts, Intrahepatic/pathology , Bile Duct Neoplasms/metabolism , Bile Duct Neoplasms/pathology , Cell Proliferation/genetics , Cell Line, Tumor , Cell Movement/genetics
2.
Biosci Rep ; 39(12)2019 12 20.
Article in English | MEDLINE | ID: mdl-31808514

ABSTRACT

BACKGROUND: The present study aimed to develop and validate a nomogram based on expanded TNM staging to predict the prognosis for patients with squamous cell carcinoma of the bladder (SCCB). METHODS: A total of 595 eligible patients with SCCB identified in the Surveillance, Epidemiology, and End Results (SEER) dataset were randomly divided into training set (n = 416) and validation set (n = 179). The likelihood ratio test was used to select potentially relevant factors for developing the nomogram. The performance of the nomogram was validated on the training and validation sets using a C-index with 95% confidence interval (95% CI) and calibration curve, and was further compared with TNM staging system. RESULTS: The nomogram included six factors: age, T stage, N stage, M stage, the method of surgery and tumor size. The C-indexes of the nomogram were 0.768 (0.741-0.795) and 0.717 (0.671-0.763) in the training and validation sets, respectively, which were higher than the TNM staging system with C-indexes of 0.580 (0.543-0.617) and 0.540 (0.484-0.596) in the training and validation sets, respectively. Furthermore, the decision curve analysis (DCA) proved that the nomogram provided superior clinical effectiveness. CONCLUSIONS: We developed a nomogram that help predict individualized prognosis for patients with SCCB.


Subject(s)
Carcinoma, Squamous Cell , Nomograms , Urinary Bladder Neoplasms , Aged , Aged, 80 and over , Carcinoma, Squamous Cell/metabolism , Carcinoma, Squamous Cell/mortality , Carcinoma, Squamous Cell/pathology , Carcinoma, Squamous Cell/surgery , Disease-Free Survival , Female , Humans , Male , Middle Aged , Neoplasm Staging , Retrospective Studies , Risk Factors , Sex Factors , Survival Rate , Urinary Bladder Neoplasms/metabolism , Urinary Bladder Neoplasms/mortality , Urinary Bladder Neoplasms/pathology , Urinary Bladder Neoplasms/surgery
3.
Int J Med Sci ; 16(5): 654-659, 2019.
Article in English | MEDLINE | ID: mdl-31217732

ABSTRACT

Bladder cancer is a common malignant urinary tumor, and patients with bladder cancer have poor prognosis. Abnormal lipid metabolism in peroxisomes is involved in tumor progression. Hydroxysteroid dehydrogenase-like 2 (HSDL2) localized in peroxisomes regulates fatty acid synthesis. In the present study, we reported that HSDL2 was upregulated in two human bladder cancer cell lines 5637 and T24 compared to normal human urothelial cells. Furthermore, lentiviral-mediated HSDL2 knockdown inhibited the proliferation and colony formation while promoted the apoptosis of human bladder cancer T24 cells in vitro. In nude mice HSDL2 knockdown inhibited the growth of T24 derived xenografts in vivo. In conclusion, our results suggest that HSDL2 plays an oncogenic role in bladder cancer and might serve as a potential target for bladder cancer therapy.


Subject(s)
Hydroxysteroid Dehydrogenases/metabolism , Oncogenes , Urinary Bladder Neoplasms/pathology , Animals , Apoptosis , Cell Line, Tumor , Cell Proliferation , Female , Gene Expression Regulation, Neoplastic , Gene Knockdown Techniques , Humans , Hydroxysteroid Dehydrogenases/genetics , Mice , Mice, Nude , RNA, Small Interfering/metabolism , Up-Regulation , Urinary Bladder/cytology , Urinary Bladder/pathology , Urinary Bladder Neoplasms/genetics , Urothelium/cytology , Urothelium/pathology , Xenograft Model Antitumor Assays
4.
Anal Biochem ; 440(1): 63-70, 2013 Sep 01.
Article in English | MEDLINE | ID: mdl-23711720

ABSTRACT

The amplification of a random single-stranded DNA (ssDNA) library by polymerase chain reaction (PCR) is a key step in each round of aptamer selection by systematic evolution of ligands by exponential enrichment (SELEX), but it can be impeded by the amplification of by-products due to the severely nonspecific hybridizations among various sequences in the PCR system. To amplify a random ssDNA library free from by-products, we developed a novel method termed single-primer-limited amplification (SPLA), which was initiated from the amplification of minus-stranded DNA (msDNA) of an ssDNA library with reverse primer limited to 5-fold molar quantity of the template, followed by the amplification of plus-stranded DNA (psDNA) of the msDNA with forward primer limited to 10-fold molar quantity of the template and recovery of psDNA by gel excision. We found that the amount of by-products increased with the increase of template amount and thermal cycle number. With the optimized template amount and thermal cycle, SPLA could amplify target ssDNA without detectable by-products and nonspecific products and could produce psDNA 16.1 times as much as that by asymmetric PCR. In conclusion, SPLA is a simple and feasible method to efficiently generate a random ssDNA sub-library for aptamer selection.


Subject(s)
Aptamers, Nucleotide/genetics , DNA, Single-Stranded/genetics , Polymerase Chain Reaction/methods , SELEX Aptamer Technique/methods , DNA Primers
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