Cancer stem cells (CSCs) markers are specific molecules to identify CSCs.Recent findings demonstrate that CSCs markers associated with colorectal cancer mainly include CD133,CD29,CD166,CD44,Nanog,etc.These markers can take park in the initiation and progression of cancers by various molecular mechanisms,which have the potential to be used as therapeutic targets as well as prognostic indicators.

As a crucial part of the DNA damage repair process,the expression of excision repair cross-complementing group 1 (ERCC1 )is closely related to the genesis and development of gastric cancer.Studies find that ERCC1 gene polymorphism can alter the expression of the gene itself,which affects the sensitivity and efficacy of platinum-based chemotherapy.Therefore,the detection of ERCC1 polymorphism may guide the indi-vidualized chemotherapy of the patients with gastric cancer.

As a member of T-box family,Tbx3 (T-box3) is widely expressed in multiple organs and involves in the development of breast,limb,heart,eye,lung and pancreas during embryonic development stage.Moreover,Tbx3 plays an important role in maintaining the embryonic stem cells.Recent studies show that Tbx3 can work as a transcription factor to participate in the initiation and progression of tumor by epithelialmesenchymal transition,induction tumor stemness and methylation.A better understanding of Tbx3 will provide new insights into genetic diagnosis and targeted treatment of tumor.

Objective To detect the expressions of Y-box-binding protein-1(YB-1)and epithelial-mesenchymal transition(EMT)markers(E-cadherin and N-cadherin)in colorectal cancer(CRC),to analyze the relationship between the expression of YB-1 and clinicopathological parameters,to evaluate the correlations among YB-1,E-cadherin and N-cadherin. Methods The expressions of YB-1,E-cadherin and N-cadherin in 120 primary CRC tumors and corresponding normal tissues were detected by western blot and immunohistochem-istry and the results were analyzed. Results The expressions of YB-1,E-cadherin and N-cadherin in tumors were significantly different from those in corresponding normal tissues(χ2 = 47. 373,P ﹤ 0. 05;χ2 = 83. 145, P ﹤ 0. 05;χ2 = 41. 832,P ﹤ 0. 05). The expression of YB-1 in tumors was associated significantly with tumor differentiation,tumor invasion,lymph node metastasis and distance metastasis(χ2 = 8. 077,P = 0. 008;χ2 =8. 178,P = 0. 006;χ2 = 15. 152,P ﹤ 0. 001;χ2 = 7. 368,P = 0. 011). It was negatively correlated with E-cadherin expression(r = - 0. 238,P = 0. 009),but positively correlated with N-cadherin expression(r =0. 361,P ﹤ 0. 001). Conclusion YB-1 may promote the occurrence and development of CRC by participating in EMT program.

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<0.05）. Overall survival rate of patients with high expression of Linc‑pint was 62.5%， which was significantly higher than that of patients with low expression of Linc‑pint （34.3%， P<0.05）. The proliferation， invasion and migration of CRC cells were inhibited after overexpression of Linc‑pint. In colorectal cancer tumor and adjacent normal tissues， Linc‑pint and miR‑21 showed opposite expression in tumor tissues and were negatively correlated （r=-0.288 and -0.908， both P<0.05）. ConclusionLinc‑pint acts as a tumor suppressor by down‑regulating the expression level of miR‑21 to inhibit the proliferation， invasion and migration of colorectal cancer.