A clinical nomogram incorporating salivary level and oral hygiene index for predicting colorectal cancer.

Background: Emerging evidence demonstrates that the salivary microbiome could serve as a biomarker for various diseases. To date, the oral microbiome's role in the diagnosis of colorectal cancer (CRC) has not been fully elucidated. We aimed to illustrate the salivary microbiome's role in diagnosing and predicting the risk of CRC.

Alterations in the oral and gut microbiome of colorectal cancer patients and association with host clinical factors.

Previous studies have suggested that gut microbiota plays a critical role in colorectal cancer (CRC). Although preliminary comparisons of the oral and gut microbiota between CRC and healthy control (HC) patients have been made, the association between microbiome abundance and host clinical factors has not been fully illustrated, especially oral health conditions. Matching samples of unstimulated saliva, cancer tissues or biopsies and stools were collected from 30 CRC and 30 HC patients from Shanghai Jiao Tong University affiliated Renji Hospital for 16S rRNA sequencing analysis.

Platelet-rich plasma inhibits Wnt/β-catenin signaling in rabbit cartilage cells activated by IL-1β.

Objective: Platelet-rich plasma (PRP) has been reported to alleviate degenerative pathological damage to joint cartilage. This study aimed to investigate the effect of PRP on Wnt/β-catenin signaling in rabbit chondrocytes.

Methods: Using 3-month-old New Zealand white rabbits, PRP was prepared from venous blood, and chondrocytes were cultured from knee joint cartilage and identified by staining for type II collagen and proteoglycan.

Probiotics Clostridium butyricum and Bacillus subtilis ameliorate intestinal tumorigenesis.

Aims: To investigate the antitumor effects of probiotics Clostridium butyricum and Bacillus subtilis on colorectal cancer (CRC) progression.

Materials & Methods: The effects of C. butyricum and B.

Inhibition of DNA methyltransferase induces G2 cell cycle arrest and apoptosis in human colorectal cancer cells via inhibition of JAK2/STAT3/STAT5 signalling.

DNA methyltransferase inhibitors (MTIs) have recently emerged as promising chemotherapeutic or preventive agents for cancer, despite their poorly characterized mechanisms of action. The present study shows that DNA methylation is integral to the regulation of SH2-containing protein tyrosine phosphatase 1 (SHP1) expression, but not for regulation of suppressors of cytokine signalling (SOCS)1 or SOCS3 in colorectal cancer (CRC) cells. SHP1 expression correlates with down-regulation of Janus kinase/signal transducers and activators of transcription (JAK2/STAT3/STAT5) signalling, which is mediated in part by tyrosine dephosphorylation events and modulation of the proteasome pathway.

RAF may induce cell proliferation through hypermethylation of tumor suppressor gene promoter in gastric epithelial cells.

The extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK-MAPK) is critical in human malignancies. It remained to be established whether DNA methyltransferases (Dnmt) and proliferating cell nuclear antigen (PCNA) involved in DNA methylation during RAF-transformed cell proliferation. The plasmid of constitutively active RAF was used to transfect gastric cell GES-1 and cancer cell AGS.

Inhibition of the extracellular signal-regulated kinase/mitogen-activated protein kinase pathway decreases DNA methylation in colon cancer cells.

The extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK-MAPK) pathway is a critical intermediary for cell proliferation, differentiation, and survival. In the human colon cancer cell line SW1116, treatment with the DNA methyltransferase 1 (DNMT1) inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) or the ERK-MAPK inhibitors PD98059 or rottlerin, or transient transfection with the MAP/ERK kinase (MEK)1/2 small interfering RNA down-regulates DNMT1 and proliferating cell nuclear antigen levels. In this report, we found that drug treatment or small interfering RNA transfection of SW1116 cells induced promoter demethylation of the p16(INK4A) and p21(WAF1) genes, which up-regulated their mRNA and protein expression levels.

[The effect of PKC-delta inhibitor Rottlerin on human colon cancer cell line SW1116 and its mechanism].

Objective: To evaluate the effect of PKC-delta inhibitor Rottlerin on human colon cancer cells and its mechanism.

Methods: Human colon cancer cell line SW1116 cells were treated with Rottlerin. The transcriptional level of DNA methyltransferase (Dnmt)1, Dnmt3a and Dnmt3b was detected by real-time RT-PCR.