a-modified-cuff-technique-for-mouse-cervical-heterotopic-heart

A Modified Cuff Technique for Mouse Cervical Heterotopic Heart Transplantation Model

Cardiac allograft rejection limits the long-term survival of patients after heart transplantation. A mouse heart transplantation model is ideal for ...

Chongqing University Cancer Hospital

BACKGROUND Recent studies have demonstrated that Linc00152 is highly expressed in multiple cancer types and its genes show tumor-promoting characteristics. However, the efficacy and biological mechanism of Linc00152 in bladder cancer remains unclear. MATERIAL AND METHODS We study investigated the relative expression and promoter methylation of Linc00152 in 126 cases of bladder cancer tissues by qRT-PCR and Bisulfite sequencing PCR. qRT-PCR was used to assess the relative expression of Linc00152 in 4 human bladder cancer cell lines. To explore the biological properties of Linc00152, we performed cell growth and soft-agar colony-formation assays, flow cytometry analyses, wound-healing assay, and Transwell assay. Western blot analysis was used to detect the underlying mechanisms of Linc00152 in bladder cancer. RESULTS We found that Linc00152 was highly expressed in 126 cases of bladder carcinoma tissues (p<0.001) and 4 cell lines (p<0.01), and Linc00152 is more commonly expressed in patients with advanced-stage cancer (p=0.021). Knockdown of Linc00152 by using siRNAs in bladder cancer cell lines (T24 and HT-1197) suppressed cell viability and growth by causing cell cycle arrest and apoptosis (p<0.001), as well as inhibiting cell migration and invasion (p<0.001). In addition, the quantitative RT-PCR and Western blot results suggest that knockdown of Linc00152 reduced Wnt/ß-Catenin signaling (p<0.001). CONCLUSIONS This research shows that Linc00152 is highly expressed in patients with bladder cancer and the possible carcinogenic effect of Linc00152 in bladder cancer occurs through activating the Wnt/ß-Catenin signaling pathway, and could be a new biomarker for diagnosis and prevention of this cancer.

Higher Expression of Linc00152 Promotes Bladder Cancer Proliferation and Metastasis by Activating the Wnt/β-Catenin Signaling Pathway.

Immunotherapy targeting programmed cell death protein 1 (PD-1)/programmed cell death-ligand 1 (PD-L1) has shown efficacy in a variety of solid tumors. However, prostate cancer has often been a non-responder to anti-PD-1/PD-L1 therapies. The objective of this study was to determine PD-1 and PD-L1 expression status and its correlation with clinical features of the patients. A total of 279 patients who underwent radical prostatectomy for prostate cancer were included in this study. PD-1 and PD-L1 expression in primary prostate tumors was detected using immunohistochemical staining. Analyses were made between PD-1/PD-L1 status and patients' age, ethnicity, body mass index (BMI), diabetes mellitus, tumor stage, lymph node metastasis, prostate-specific antigen (PSA), Gleason score, grade group, and survival. We found that 6.5 (standard deviation 14.3; range 0-161.6) tumor-infiltrating lymphocytes per high power field were positive for PD-1 staining and 50/279 (17.9%) tumors were positive for PD-L1 staining. PD-L1-positive tumors had significantly more PD-1-positive lymphocytes than PD-L1-negative tumors. The number of PD-1-positive lymphocytes was not correlated with any clinical features except that patients with diabetes had significantly less PD-1-positive lymphocytes than patients without diabetes. In contrast, more PD-L1-positive tumors were found in older patients (≥ 65 years), obese patients (BMI ≥ 30), and patients with advanced tumor stage, lymph node metastasis, and high Gleason score. Neither PD-1 nor PD-L1 status was correlated with ethnicity, PSA, or survival. Our findings suggest that PD-L1 instead of PD-1 status is associated with the clinical features in human primary prostate tumors.

PD-L1 instead of PD-1 status is associated with the clinical features in human primary prostate tumors.

Bladder cancer (BC) is one of the most prevalent malignancies of the genitourinary system, yet the underlying mechanism of BC progression still remains unclear. Growth arrest and DNA damage-inducible 45 alpha (GADD45a) is a repressive gene implicated in cell cycle regulation, as well as in human cancers development. However, its role in BC remains to be determined.

GADD45a Mediated Cell Cycle Inhibition Is Regulated By P53 In Bladder Cancer.

The efficacy and safety of prostate SBRT in men with mCRPC is unknown.

Article	Year
Higher Expression of Linc00152 Promotes Bladder Cancer Proliferation and Metastasis by Activating the Wnt/β-Catenin Signaling Pathway. Medical science monitor : international medical journal of experimental and clinical research\| PubMed ID: 31042695	2019
PD-L1 instead of PD-1 status is associated with the clinical features in human primary prostate tumors. American journal of clinical and experimental urology\| PubMed ID: 31317055	2019
GADD45a Mediated Cell Cycle Inhibition Is Regulated By P53 In Bladder Cancer. OncoTargets and therapy\| PubMed ID: 31571910	2019
Efficacy and safety of Prostate stereotactic body radiotherapy for metastatic castration-resistant prostate cancer: A prospective cohort study. Cancer treatment and research communications\| PubMed ID: 33848805	2021

Peng Xian

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