RESUMEN
Long non-coding RNAs (LncRNAs) are abnormally expressed in a variety of tumors and participate in the occurrence and development of tumors. However, the expression and function of many LncRNAs in tumors have not been fully clarified. In this paper, 113 normal breast tissues and 1 109breast cancer tissues were analyzed in TCGT database. LncRNA AL133467. 1 was found to be lowly expressed in breast cancer tissues and negatively correlated with poor prognosis of breast cancer patients. The expression of AL133467. 1 in breast cancer cells was significantly lower than that in normal breast epithelial cells. We overexpressed AL133467. 1 in relatively low-expression breast cancer cells SKBR3and BT474, and cell count and plate colony-formation experiments showed that overexpression ofAL133467. 1 could significantly inhibit the proliferation and colony formation of breast cancer cells (P< 0. 01). Cell scratch and Transwell assays showed that the migration and invasion ability of breast cancer cells overexpressing AL133467. 1 was significantly reduced compared with the control group (P<0. 01). MiRDB database showed that AL133467. 1 had binding sites with miR-661. miR-661 could bind the transducer of ErbB2, 2 (ErbB2, 2, TOB2). qRT-PCR showed that miR-661 was highly expressed inbreast cancer cells and positively correlated with poor prognosis of breast cancer patients (P < 0. 001). Luciferase reporter assays showed that AL133467. 1 had specific binding to miR-661 (P < 0. 01). AL133467. 1 overexpression could inhibit the expression of miR-661 in breast cancer cells (P<0. 0001). Transfection of miR-661 mimics eliminated the inhibitory effect of overexpression of AL133467. 1 on breast cancer cells (P < 0. 001). In addition, qRT-PCR and Western blotting results showed that overexpression of AL133467. 1 up-regulated TOB2 mRNA (P < 0. 0001) and protein levels. But whenmiR-661 mimics were transfected, TOB2 mRNA (P < 0. 0001) and protein levels were significantly inhibited. In conclusion, as a competitive endogenous RNA of miR-661. AL133467. 1 promotes the expression of TOB2, thereby inhibiting the proliferation and invasion of breast cancer cells.
RESUMEN
Long non-coding RNAs (LncRNAs) , as regulators of a class of gene expression, play a key role in the development of various types of tumor.We analyzed the TCGA database and found that the expression of LncRNA AC009686.2 in breast cancer tissues was significantly higher than that in normal tissues, and was positively correlated with the poor prognosis of breast cancer patients.qRT-PCR analysis showed that the expression of LncRNA AC009686.2 in breast cancer cells was significantly up-regulated, and the expression level of LncRNA AC009686.2 in MCF7, T47D, ZR7530, BT549, HCC1937, MDA- MB-231 and SKBR3 eells was 6.58, 5.66, 7.29, 9.06, 6.89, 11.17 and 5.38 folds of that in MCF10 A eells, respectively.LncRNA AC009686.2 knockdown in MDA-MB-231 and BT549 cells which expressed relatively high LncRNA AC009686.2 significantly inhibited cell proliferation, colony formation and invasion, and induced cell G,/S phase arrest.The clone inhibition rates of MDA-MB-231 and BT549 cells with LncRNA AC009686.2 knockdown were 0.496%, 0.438% and 0.495%, 0.353% of the control group, respectively.LncRNA AC009686.2 knockdown also down-regulated protein levels of cyclinD2 and ZEB1.However, overexpression of ZEB1 could significantly reverse the decrease of cell invasion ability caused by LncRNA AC009686.2 knockdown.We further analvsed in the software JASPAR database and found that LncRNA AC009686.2 promoter had ZEB1 binding site, and overexpression of ZEB1 could down-regulate the expression level of LncRNA AC009686.2 in breast cancer cells.In conclusion, LncRNA AC009686.2 which highly expressed in breast cancer, promotes cell proliferation and invasion by up-regulating cyclinD2 and ZEB1 expression, while ZEB1 positively regulates LncRNA AC009686.2 expression.This study will provide a theoretical basis for elucidating the role of LncRNA AC009686.2 in breast cancer and related molecular mechanisms.
RESUMEN
<p><b>OBJECTIVE</b>To evaluate the efficacy of hypofractionated radiotherapy combined with docetaxel for treatment of bone metastasis of lung cancer and explore the factors related to the prognosis.</p><p><b>METHODS</b>Seventy-two patients with bone metastasis of lung cancer were divided into group A with hypofractionated radiotherapy at 3.0 Gy /fraction (once a day, 5 days per week for 30 Gy) and weekly docetaxel treatment at 60 mg for 2 weeks, and group B with radiotherapy alone at 2.0 Gy/fraction (once a day, 5 days per week for 40 Gy).</p><p><b>RESULTS</b>The total effective rate was 93.1% (67/72) in these patients, with a non-response rate of 6.9% (5/72). The total effective rate was 97.2% (35/36) in group A and 88.9% (32/36) in group B. After the radiotherapy, the analgesic effect showed no significant difference between the two groups, but the onset of the effect was faster in group B than in group A.</p><p><b>CONCLUSION</b>Local radiotherapy provides effective pain relief in patients with bone metastasis of lung cancer. High-dose fractionated irradiation can rapidly achieve the analgesic effect.</p>