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ObjectiveTo investigate the biological function and molecular mechanism of long non-coding RNA Linc‑pint in colorectal cancer.MethodsQuantitative real‑time quantitative （qRT‑PCR） was performed to detect the expression level of Linc‑pint in 31 pairs of colorectal cancer tumor and adjacent normal tissues； correlation between the expression level of Linc‑pint and the clinicopathological characteristics was analyzed by the chi‑square test. Kaplan-Meier survival analysis was used to assess the relationship between Linc‑pint expression level and the prognosis of patients. Cox regression model was used to analyze the relationship between clinicopathological characteristics and the prognosis of patients. Expression level of Linc‑pint were detected by qRT‑PCR in 5 common colorectal cancer cell lines. Effect of Linc‑pint on cell proliferation， invasion and migration was measured by cell counting kit‑8 assay， Transwell assay and harvested xenografts from nude mice. qRT‑PCR was performed to detect the expression level of Linc‑pint's target gene micro RNA（miR）‑21 in 31 pairs of colorectal cancer tumor tissues and adjacent normal tissues. Pearson correlation coefficient was used to assess the correlation between Linc‑pint and miR‑21. qRT‑PCR was used to detect the expression of overexpression of Linc‑pint on miR‑21 in colorectal cancer cells.ResultsExpression level of Linc‑pint in normal tissues （3.95±1.16） was significantly higher than that in colorectal cancer tissues （2.74±0.95） （t=6.17， P

Abstract: Colorectal cancer (CRC) is a common human malignancy worldwide and increasing studies have attributed its malignant progression to abnormal molecular changes in cancer cells. Nuclear division cycle 80 (NDC80) is a newly discovered oncoprotein that regulates cell proliferation and cycle in numerous malignancies. However, its clinical significance and biological role in CRC remain unclear. Therefore, in this study, we firstly analyze its expression in a retrospective cohort enrolling 224 CRC patients and find its overexpression is significantly correlated with advanced tumor stage and poor prognosis in CRC patients. In addition, our result reveals it is an independent adverse prognostic factor affecting CRC‐specific and disease‐free survival. The subgroup analysis indicates NDC80 expression can stratify the clinical outcome in stage II and III patients, but fails in stage I and IV patients. In cellular assays, we find knockdown of NDC80 dramatically inhibits the proliferative ability, apoptosis resistance, cell cycle progression, and clone formation of CRC cells in vitro. Using xenograft model, we further prove knockdown of NDC80 also inhibits the tumorigenic ability of CRC cells in vivo. Finally, the microarray analysis is utilized to preliminarily clarify the oncogenic molecular mechanisms regulated by NDC80 and the results suggest it may promote CRC progression partly by downregulating tumor suppressors such as dual specificity phosphatase 5 and Forkhead box O1. Taken together, our study provides novel evidences to support that NDC80 is not only a promising clinical biomarker but also a potential therapeutical target for CRC precise medicine. [ABSTRACT FROM AUTHOR]

T-cell leukemia/lymphoma-1A (TCL1A) as a stem cell marker is abundantly expressed in embryonic stem cells and has been identified as an oncogene in various hematological malignancies such as chronic lymphocytic leukemia and B-cell lymphoma. However, with regard to its role in solid tumors, few studies are available and less are for colorectal cancer (CRC). In this study, we aim to investigate the expression and clinical significance of TCL1A in a cohort of 278 stage II/III CRC patients. As a result, we find TCL1A expression is higher in CRC tissues than that in adjacent normal tissues, and significantly correlated with tumor differentiation, TNM stage and Ki-67 positive rate. The prognostic analysis suggests that TCL1A expression is an independent factor affecting CRC-specific and disease-free survival of these patients. Furthermore, we find stage II/III patients with high TCL1A expression have a significantly higher rate of postoperative local recurrence and metastasis than those with low TCL1A expression. Finally, through subgroup analysis, we find TCL1A expression can stratify the outcome of stage II/III patients who received standard adjuvant chemotherapy. Taken together, our findings suggest TCL1A is not only a useful biomarker for prognostic evaluation in stage II/III CRC patients, but also a promising therapeutic target for improving their clinical outcome. [ABSTRACT FROM AUTHOR]