AL360181.1 promotes proliferation and invasion in colon cancer and is one of ten m6A-related lncRNAs that predict overall survival.

Background: N6-methyladenosine (m6A) exerted a pivotal role in colon cancer. Nevertheless, the long non-coding RNAs (lncRNAs) associated with this process have yet to be elucidated. Methods: The open-access data used for analysis was downloaded from The Cancer Genome Atlas (TCGA) database for analysis, employing the R software for computational evaluations. The RNA level of specific molecules was assessed using the quantitative real-time PCR. CCK8, colony formation and transwell assay were used to evaluate the proliferation, invasion and migration ability of colon cancer cells. Results: Here, we identified the m6A regulators from TCGA data and subsequently pinpointed lncRNAs with a -Cor- > 0.3 and P < 0.05, categorizing them as m6A-associated lncRNAs. Moreover, we formulated a prognosis signature rooted in ten m6A-related lncRNAs, consisting of AL360181.1, PCAT6, SNHG26, AC016876.1, AC104667.2, AL114730.3, LINC02257, AC147067.1, AP006621.3 and AC009237.14. This signature exhibited notable predictive accuracy in gauging patient survival. Immune-related evaluations revealed varied immune cell infiltration patterns across different risk groups, with our findings suggesting superior immunotherapy response in low-risk patients. Biological enrichment analysis indicated that the high-risk patients had a higher activity of multiple carcinogenic pathways, including glycolysis. The previously unreported lncRNA, AL360181.1, displayed a connection to glycolytic activity and diminished survival rates, warranting further investigation. The result indicated that AL360181.1 was correlated with more aggressive clinical characteristics. Immune infiltration assessments found AL360181.1 to have a positive correlation with Tcm infiltration, but an inverse relationship with entities like Th2 cells, T cells, neutrophils and macrophages. Biological enrichment analysis indicated that the pathways of WNT/ß-catenin, pancreas beta cells, hedgehog signaling and some metabolism pathways were upregulated in high AL360181.1 patients. In vitro experiments showed that AL360181.1 was upregulated in the colon cancer cells. Moreover, AL360181.1 significantly promotes the proliferation, invasion and migration of colon cancer cells. Conclusions: Our results can provide direction for future studies on m6A-related lncRNA in colon cancer.

Idiopathic mesenteric phlebosclerosis: one case report and systematic literature review of 240 cases.

AIM: This research is both a case study and a systematic literature review. Our goal was to learn more about the pathophysiology, clinical features, and therapy options for idiopathic mesenteric phlebosclerosis (IMP). METHODS: A case of IMP was treated by surgery in our department. Combined with the data of 240 cases of IMP retrieved from PubMed and Wanfang Data, we conducted a systematic review of this less well-known disease. RESULTS: These 240 cases of IMP mainly occurred in East Asia. Among the patients, 78.7% of them had a history of herbal medicine consumption; 15.2% had no obvious symptoms and their diagnosis was confirmed through characteristic CT findings and colonoscopic manifestations; 58.4% were cured by conservative treatment; 41.6% had severe symptoms and underwent surgical treatment. Additionally, more patients treated with surgical treatment had lesions involving the cecum (59/82 vs. 53/115, P=0.0003) and sigmoid colon (20/82 vs. 10/115, P=0.0025) compared with those treated conservatively. CONCLUSION: The occurrence of IMP is associated with the long-term consumption of herbal medicines. Early diagnosis of IMP could be determined by CT and colonoscopy and conservative or surgical treatment was chosen based on of the severity of the condition (e.g., the involved bowel segment).

Clinical significance and biological role of KLF17 as a tumour suppressor in colorectal cancer.

It has been reported that kruppel­like factor 17 (KLF17) acts as a tumour suppressor in several tissues and cancer cells, however, the molecular roles, the underlying mechanisms and clinical significance of KLF17 in colorectal cancer (CRC) have not been completely elucidated. In the present study, KLF17 protein expression was detected in 140 primary CRCs and paired adjacent non­tumour tissues using immunohistochemistry with tissue microarrays. The KLF17 mRNA expression was determined in 4 CRC cell lines and 20 pairs of the aforementioned tissues using reverse transcription quantitative polymerase chain reaction. The correlation between KLF17 expression and clinicopathologic characteristics was determined. Next, the functions of KLF17 in CRC were examined by cell proliferation, colony formation, adhesion, invasion and mouse xenograft assays. Methylation­specific PCR and bisulfite sequencing PCR were also carried out to investigate the promoter methylation status of KLF17 in CRC cells and tissues and explore the effects of lentiviral­mediated RNAi of UHRF1 on the methylation and expression of KLF17. The results revealed that KLF17 expression was abnormally decreased in CRC and associated with lymph node metastasis and unfavorable overall survival. Moreover, ectopic KLF17 expression suppressed CRC cell growth and invasion in vitro and in vivo. In addition, the downregulation of KLF17 was associated with the hypermethylation of the CpG nucleotides on the KLF17 promoter. The knockdown of the epigenetic regulator UHRF1 reduced the methylation level of the KLF17 promoter and inhibited CRC cell adhesion, invasion and epithelial­mesenchymal transition by upregulating KLF17. The present findings indicated that KLF17 may act as a tumour suppressor gene in CRC and a potential independent prognostic biomarker in CRC patients. UHRF1 can suppress KLF17 expression through the hypermethylation of its promoter in CRC. These results offer insights into the KLF17 expression regulation in CRC and suggest an inhibitory effect of KLF17 on tumourigenesis.