LncRNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells / 한국유방암학회지

PURPOSE: This study was designed to investigate the role of taurine-upregulated gene 1 (TUG1) in MCF-7 breast cancer cells and the molecular mechanism involved in the regulation of microRNA-9 (miR-9). METHODS: The expression of TUG1 in breast cancer tissues and cells was evaluated using quantitative reverse transcription polymerase chain reaction. Cell viability was examined using a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay; cell cycle progression and apoptosis were analyzed using flow cytometry. A dual luciferase reporter assay was used to detect the relationship between TUG1 and miR-9. The expression of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was measured by western blot. RESULTS: Higher expression of TUG1 was observed in breast cancer tissues and cell lines than in the corresponding controls. TUG1 knockdown reduced proliferation, suppressed cell cycle progression, and promoted apoptosis of MCF-7 cells. The dual luciferase reporter assay showed that TUG1 could negatively regulate the expression of miR-9. MiR-9 inhibition abrogated the effect of TUG1 knockdown on the proliferation, cell cycle progression, and apoptosis of MCF-7 cells. TUG1 positively regulated the expression of MTHFD2 in breast cancer cells. CONCLUSION: TUG1 knockdown was significantly associated with decreased cell proliferation and it promoted apoptosis of breast cancer cells through the regulation of miR-9.

Bilateral chylothorax following left supraclavicular lymph node dissection for breast cancer: one case report and literature review / 癌症

Chylothorax is a rare complication of neck dissection, and bilateral chylothorax is even rarer. However, both are potentially serious and sometimes life-threatening, especially those that are associated with left neck dissection for head and neck neoplasms. We report one case of bilateral chylothorax following left supraclavicular dissection for breast cancer. This case was treated successfully with a new conservative management approach.

Aberrant promoter CpG methylation and its translational applications in breast cancer / 癌症

Breast cancer is a complex disease driven by multiple factors including both genetic and epigenetic alterations. Recent studies revealed that abnormal gene expression induced by epigenetic changes, including aberrant promoter methylation and histone modification, plays a critical role in human breast carcinogenesis. Silencing of tumor suppressor genes (TSGs) by promoter CpG methylation facilitates cells growth and survival advantages and further results in tumor initiation and progression, thus directly contributing to breast tumorigenesis. Usually, aberrant promoter methylation of TSGs, which can be reversed by pharmacological reagents, occurs at the early stage of tumorigenesis and therefore may serve as a potential tumor marker for early diagnosis and therapeutic targeting of breast cancer. In this review, we summarize the epigenetic changes of multiple TSGs involved in breast pathogenesis and their potential clinical applications as tumor markers for early detection and treatment of breast cancer.

Effect of small interfering RNA targeting CXCR4 on breast cancer angiogenesis / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effects of a small interfering RNA targeting CXCR-4 (shRNA-CXCR4) on angiogenesis of human breast cancer cells.</p><p><b>METHODS</b>The expression of CXCR4 mRNA and protein in 3 breast cancer cell lines with CXCR-4 silencing mediated by shRNA-CXCR4 was detected by RT-PCR and Western blotting, respectively. The morphological changes of human umbilical vein endothelial cells (HUVECs) were observed in co-culture with human breast cancer cells after CXCR4 gene silencing.</p><p><b>RESULTS</b>CXCR4 mRNA and protein expressions decreased significantly in MCF-7, MDA-MB-231 and MDA-MB-435s breast cancer cells after the gene silencing (P<0.05). Gene silencing with shRNA-CXCR4 in human breast cancer cells significantly inhibited the ability of HUVECs to form tubular structures in the co-culture (P<0.05).</p><p><b>CONCLUSION</b>Gene silencing by shRNA-CXCR4 can obviously lower the angiogenesis-inducing ability of human breast cancer cells.</p>

Comparison of hyaluronidase expression, invasiveness and tubule formation promotion in ER (-) and ER (+) breast cancer cell lines in vitro / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hyaluronidase (Hyase) is an enzyme which hydrolyses hyaluronan (HA), a large nonsulfated glycosaminoglycan. Several genes have been identified to code for hyaluronidases in humans. Its role has only recently been underlined in the invasion of prostate cancer, colonic cancer, and breast cancer. Moreover, the findings were in agreement with some experimental results which showed that HA-derived oligosaccharides had angiogenesis-promoting activity. All these findings prompted us to investigate factors that had been characterized as putative invasive factors in different human breast cancer-derived cell lines.</p><p><b>METHODS</b>We selected two series of human breast cancer-derived cell lines whose expression of estrogen receptors (ER) was previously published. Hyaluronidase secretion in culture medium and expression of matrix metallo-proteinase (MMP)-9, cathepsin-D (cath-D) and vascular endothelial growth factor (VEGF) by cells were determined. We also investigated cell invasiveness in the Matrigel invasion assay, and studied the capability of cancer cells to promote in vitro formation of tubules by endothelial cells.</p><p><b>RESULTS</b>ER(-) cells secreted significantly more hyaluronidase (P < 0.001) and expressed significantly more VEGF (P < 0.01), MMP-9 (P < 0.05) and cath-D (P < 0.0001) than ER(+) cells. Invasion through Matrigel by ER(-) Hyase(+) cells was significantly higher than that by ER(+) Hyase(-) cells (P < 0.05). In both cases, invasion was decreased by heparin (P < 0.05). When ECV-304 endothelial cells were co-cultivated in millicell chambers with cancer cells, ECV-304 cells were induced to form tubules. Tubule formation was demonstrated to be more prominent with ER(-) Hyase(+) cells than with ER(+) Hyase(-) cells (P < 0.05).</p><p><b>CONCLUSION</b>Invasive features of ER(-) breast cancer cells can be characterized in vitro by an invasive Matrigel assay, as the induction of tubule formation by ECV-304 endothelial cells, higher secretion of hyaluronidase, and higher expression of proteinases MMP-9, cath-D, and the angiogenesis promoting factor VEGF.</p>

A follow-up study about 52 cases of atypical lobular hyperplasia and lobular carcinoma in situ of the breast / 中华外科杂志

<p><b>OBJECTIVE</b>To evaluate the biological behavior and treatment method for the breast atypical lobular hyperplasia (ALH) and breast lobular carcinoma in situ (LCIS).</p><p><b>METHODS</b>Seventeen cases of ALH and thirty-five cases of LCIS were reviewed from July 1982 to January 1996. All cases were followed by physical examination, mammography and B-ultrasound for an average of 146.6 months (range, 3 - 257 months).</p><p><b>RESULTS</b>Most cases of ALH and LCIS occurred before menopause (about 69.2%). Fifty-two cases of ALH and LCIS were occasionally verified pathologically after surgery for benign diseases. The microcalcification with ALH and LCIS had been detected in 25 cases, accounted for 48.1%. Eight cases of ALH/LCIS became invasive carcinoma. There were 5 cases in the same breast, 3 cases in the contralateral breast; The subsequent breast cancer occurred longer than nine years after ALH/LCIS was diagnosed. The family history of breast carcinoma and ovary carcinoma occurred in 4 cases of breast carcinoma, accounted for 50%, but it was no significant (P > 0.05). Also, there was no difference between LCIS and ALH, which occurred the breast carcinoma (P > 0.05).</p><p><b>CONCLUSION</b>The excisional biopsy might be necessary to ALH and LCIS.</p>