Tumor microenvironment B cells increase bladder cancer metastasis via modulation of the IL-8/androgen receptor (AR)/MMPs signals

Bladder cancer is a menace to global health worldwide due to its high recurrence rate and its progression to invasive muscular complications. Cell adhesion molecules play an intricate role in cancer migration, growth, and invasion. Therefore, through bioinformatics analysis, it was found that the higher cerebral endothelial cell adhesion molecule (CERCAM) predicted lower chance in bladder cancer patient survival; subsequently, in vitro and in vivo investigations were performed to evaluate the specific effects of CERCAM on bladder cancer cell phenotypes and tumor growth in mice model. The PCR-based analysis revealed an aberrant upregulation of CERCAM in bladder carcinoma tissues and cells when compared with normal controls. In vitro, functional experiments such as MTT, EdU, and Transwell assays showed that CERCAM overexpression markedly enhanced bladder cancer cell viability, DNA synthesis, and cell invasion. In contrast, CERCAM silencing suppressed bladder cancer cell viability, DNA synthesis, and cell invasion. CERCAM overexpression significantly increased PCNA, Vimentin, Twist, and N-cadherin proteins but decreased E-cadherin and cleaved-caspase3, whereas CERCAM silencing exerted opposite effects on these markers. In vivo, subcutaneous implant model experiments in nude mice showed that CERCAM silencing suppressed the growth of subcutaneously implanted tumors. CERCAM altered the phosphorylation process of AKT. The PI3K inhibitor LY294002 treatment manifested similar effects as CERCAM silencing on bladder cancer cell behaviors and partially impaired the promotive functions of CERCAM overexpression upon the capacity of bladder cancer cells to proliferate and invade. When taken together, the cell adhesion molecule CERCAM is overexpressed in bladder cancer tissues. In vitro, CERCAM overexpression significantly promoted bladder cancer cell viability, DNA synthesis, and cell invasion and alters the cleaved-caspase3, E-cadherin, and N-cadherin expression pattern; in vivo, CERCAM silencing suppressed tumor growth in nude mice. The PI3K/AKT signaling is suspected of interfering participate in the functions of CERCAM in bladder carcinoma.

Endocrine neoplasms remain a great threat to human health. It is extremely important to make a clear diagnosis and timely treatment of endocrine tumors. Machine learning includes radiomics, which has long been utilized in clinical cancer research. Radiomics refers to the extraction of valuable information by analyzing a large amount of standard data with high-throughput medical images mainly including computed tomography, positron emission tomography, magnetic resonance imaging, and ultrasound. With the quantitative imaging analysis and model building, radiomics can reflect specific underlying characteristics of a disease that otherwise could not be evaluated visually. More and more promising results of radiomics in oncological practice have been seen in recent years. Radiomics may have the potential to supplement traditional imaging analysis and assist in providing precision medicine for patients. Radiomics had developed rapidly in endocrine neoplasms practice in the past decade. In this review, we would introduce the general workflow of radiomics and summarize the applications and developments of radiomics in endocrine neoplasms in recent years. The limitations of current radiomic research studies and future development directions would also be discussed.