Long noncoding RNA LINC00184 facilitates the proliferation, metastasis, and adenine metabolism of cholangiocarcinoma via modulating hsa-miR-23b-3p/ANXA2 axis.

The purpose of this article was to probe the mechanism underlying long noncoding RNA (lncRNA)-LINC00184 in cholangiocarcinoma development and to investigate the effects of LINC00184 on cholangiocarcinoma. We used bioinformatics to analyze the expression of LINC00184, microRNA (miR)-23b-3p and ANXA2 in cholangiocarcinoma tissues. The levels of LINC00184, miR-23b-3p, and ANXA2 were detected by qRT-PCR. Cell proliferation was tested by CCK8. Transwell assay was used to detect cell invasion and migration. The target connection between LINC00184, miR-23b-3p, or ANXA2 was probed by luciferase reporter assay. RNA pull-down method was employed to test the relationship among LINC00184/miR-23b-3p/ANXA2 in cholangiocarcinoma cells. The Pearson correlation coefficient analyzed was applied to analyze the correlation among LINC00184, miR-23b-3p, and ANXA2. LC-MS/M analysis was used to explore whether the changes of adenine metabolism was affected by LINC00184 in cholangiocarcinoma cells. We discovered that LINC00184 expression was heightened in cholangiocarcinoma patients and cells. Knockdown of LINC00184 repressed cell proliferation, invasion, migration and adenine metabolism in cholangiocarcinoma cells. miR-23b-3p was regarded as a target of LINC00184 and its depletion perversed the inhibitive influence of LINC00184 silencing on cholangiocarcinoma cells. ANXA2 was a target of miR-23b-3p and was negatively modulated by miR-23b-3p. Moreover, ANXA2 was positively modulated by LINC00184 via sponging miR-23b-3p. In short, silencing of LINC00184 suppressed cell proliferation, invasion and migration through over-expression of miR-23b-3p and reducing of ANXA2 in cholangiocarcinoma cells. These findings contribute to understanding the influences of LINC00184, miR-23b-3p, and ANXA2 on cholangiocarcinoma and provide basis for cholangiocarcinoma treatment.

Morphologic features of lymphatic in periphery region of gastric carcinoma and colon carcinoma.

BACKGROUND & OBJECTIVE: Most of the studies on lymphatic metastasis mechanism of carcinoma are confined to distribution of lymphatics. This research was to observe distribution and morphologic features of the lymphatics in periphery region of carcinoma, and morphologic changes of lymphatic endothelia. METHODS: Specimens were obtained from 10 patients with gastric carcinoma and 10 patients with colon carcinoma; 20 mice models bearing colon carcinoma were established. Morphology of lymphatics and ultrastructure of lymphatic endothelia were observed under microscope. Number density and volume density of lymphatics in periphery region of carcinoma and normal region were measured using computer image analysis system; open rate and destructive rate of lymphatics were calculated. RESULTS: The lymphatics in periphery region of carcinoma were dilated; their walls were disintegrated. Lymphatic endothelia were dissolved and destroyed into broken fragments; the organellae showed pathologic changes. Number density and volume density of lymphatics were significantly higher in periphery region of colon carcinoma than in normal region [(10.2+/-1.7)/mm(2) vs. (5.1+/-0.8)/mm(2), P < 0.05û (1.5+/-0.2)% vs. (0.7+/-0.0)%, P < 0.05], and were significantly higher in periphery region of gastric carcinoma than in normal region [(8.0+/-0.9)/mm(2) vs. (3.4+/-0.6)/mm(2), P < 0.01; (1.6+/-0.3)% vs. (0.8+/-0.2)%, P < 0.05]. Open rate of lymphatics was significantly higher in periphery regions of mice model colon carcinoma, human gastric carcinoma, and colon carcinoma than in relevant normal regions (22.2% vs. 7.8%, 35.0% vs. 8.0%, and 25.8% vs. 5.0%, P < 0.05). Destructive rate of lymphatics was significantly higher in periphery regions of mice model colon carcinoma, and human gastric carcinoma than in relevant normal regions (20.1% vs. 0, and 35.3% vs. 2.0%, P < 0.05). CONCLUSION: Compare with the lymphatics in normal tissue, the lymphatics in periphery region of carcinoma tissue are dilated with disintegrated walls; the lymphatic endothelia are destroyed; the density of the lymphatics is increased.