Fucoidan from Sargassum hemiphyllum inhibits the stemness of cancer stem cells and epithelial-mesenchymal transitions in bladder cancer cells.

A variety of anticancer activities have been established for fucoidan from brown algae, whereas whether cancer stem cells (CSCs) are inhibited by sulfated polysaccharides is unexplored. In this study, fucoidan extracted from Sargassum hemiphyllum was showed heat stable and might tolerate 140 °C treatment. Fucoidan did not exhibit cytotoxicity in 5637 and T24 bladder cancer cells.

Effects of nerve-sparing procedures on surgical margins after robot-assisted radical prostatectomy.

Background: Nerve-sparing (NS) techniques could potentially increase positive surgical margins after robot-assisted radical prostatectomy (RARP). Nevertheless, the available studies have revealed ambiguous results among distinct groups. This study purposed to clarify the details of NS techniques to accurately estimate their influence on margin status.

Prediction of a positive surgical margin and biochemical recurrence after robot-assisted radical prostatectomy.

The positive surgical margin (PSM) and biochemical recurrence (BCR) are two main factors associated with poor oncotherapeutic outcomes after prostatectomy. This is an Asian population study based on a single-surgeon experience to deeply investigate the predictors for PSM and BCR. We retrospectively included 419 robot-assisted radical prostatectomy cases.

Bioapplications of Bacterial Cellulose Polymers Conjugated with Resveratrol for Epithelial Defect Regeneration.

Excellent wound dressing is essential for effective wound repair and regeneration. However, natural polymeric skin substitutes often lack mechanical strength and hydrophilicity. One way to overcome this limitation is to use biodegradable polymers with high mechanical strength and low skin-irritation induction in wet environments.

Down-regulation of BNIP3 by olomoucine, a CDK inhibitor, reduces LPS- and NO-induced cell death in BV2 microglial cells.

Proinflammatory responses eliciting the microglial production of cytokines and nitric oxide (NO) have been reported to play a crucial role in the acute and chronic pathogenic effects of neurodegeneration. Chemical inhibitors of cyclin-dependent kinases (CDKs) may prevent the progression of neurodegeneration by both limiting cell proliferation and reducing cell death. However, the mechanism underlying the protective effect of CDK inhibitors on microglia remains unexplored.

Galectin-1 upregulates CXCR4 to promote tumor progression and poor outcome in kidney cancer.

Galectin-1, a β-galactoside-binding lectin, is involved in many physiologic and pathologic processes, including cell adhesion, differentiation, angiogenesis, and tumor progression. However, the role of galectin-1 in kidney cancer remains elusive. This study evaluated the role of galectin-1 in the progression and clinical prognosis of renal cell carcinoma.

Autocrine CCL2 promotes cell migration and invasion via PKC activation and tyrosine phosphorylation of paxillin in bladder cancer cells.

The amount of monocyte chemoattractant protein-1 (MCP-1/CCL2) produced by a transitional cell carcinoma is directly correlated with high recurrence and poor prognosis in bladder cancer. However, the mechanisms underlying the effects of CCL2 on tumor progression remain unexplored. To investigate the role played by CCL2, we examined cell migration in various bladder cancer cell lines.

Pre-existing Fas ligand (FasL) in cancer cells elicits tumor-specific protective immunity, but delayed induction of FasL expression after inoculation facilitates tumor formation.

Overexpression of Fas ligand (FasL) in cancer cells elicits potential antitumor effects via recruitment of neutrophils. Conversely, FasL-expressing tumors may counterattack tumor-infiltrating lymphocytes by delivering apoptotic death signals via Fas/FasL interactions, which may lead to tumor escape. In order to distinguish the role of FasL in antitumor activity and tumor progression, Lewis lung carcinoma cells (LLC-1) were used to establish the cell line LLC-FasL, in which FasL expression was repressed by doxycycline (Dox) treatment and induced in the absence of Dox.

Tumor necrosis factor-α induces epithelial-mesenchymal transition of renal cell carcinoma cells via a nuclear factor kappa B-independent mechanism.

Chronic low dose of tumor necrosis factor-α (TNF-α) stimulation promotes tumorigenesis by facilitating tumor proliferation and metastasis. The plasma levels of TNF-α are increased in patients with renal cell carcinoma (RCC). Furthermore, high-grade clear cell RCC cell lines secrete more TNF-α than low-grade ones, and allow low-grade cell lines' gain of invasive ability.