[Long noncoding RNA Linc00662 promotes the tumorigenesis of prostate cancer cells].

OBJECTIVE: To investigate the expression of Linc00662 in PCa and its influence on the biological function of PCa cells. METHODS: Using qRT-PCR, we detected the expression of Linc00662 in the PCa tissue and cell lines and that in the adjacent normal prostatic tissue and epithelial WPMY-1 cells and analyzed the correlation between the expression of Linc00662 and the clinicopathological features of the PCa tissue. We transfected PC-3 and DU145 cells with siRNA, and verified the interference efficiency by qRT-PCR. We examined the effects of interfering with the Linc00662 expression on the proliferation, apoptosis, migration and invasiveness of PC-3 and DU145 cells by CCK-8 assay, Caspase 3/9 activity assay, wound-healing assay and Transwell invasion assay. RESULTS: The expression of Linc00662 in the PCa tissue and cell lines was significantly up-regulated compared with that in the adjacent normal prostatic tissue and epithelial cells (P < 0.01), and the high expression of Linc00662 was positively correlated with the tumor stage (P = 0.002), primary tumor size (P = 0.006), lymph node metastasis (P = 0.001) and distant metastasis (P = 0.001). Transfection of si-Linc00662 into the PC-3 and DU145 cells significantly reduced the expression of Linc00662 (P < 0.01). Compared with the normal control, the PC-3 and DU145 cells in the Linc00662 interference group showed remarkably decreased proliferation, invasion and migration abilities (P < 0.01), but an increased rate of apoptosis (P < 0.01). CONCLUSIONS: Linc00662 is highly expressed in PCa tissues and cells relatively. Knockdown of the Linc00662 expression may inhibit the proliferation, migration and invasiveness and promote the apoptosis of PCa cells. Therefore, Linc00662 could be considered as a new marker of PCa.

Long intergenic non-coding RNA LINC00662 contributes to malignant growth of colorectal cancer cells by upregulating c-myc via sponging microRNA-145.

Long non-coding RNAs (lncRNAs) have appeared as vital regulatory factors in different pathological processes, particularly in tumorigenesis. Increasing number of evidence has demonstrated that long intergenic non-coding RNA 00662 (LINC00662) is overexpressed in several types of cancers and promotes cancer initiation and development. However, whether LINC00662 participates in colorectal cancer (CRC) remains unclear. This study was aimed to explore the expression, biological function and regulatory mechanism of LINC00662 in CRC. Here, we found that LINC00662 expression was obviously upregulated in CRC tissues and cell lines. Down-regulation of LINC00662 dramatically inhibited the growth of CRC cells and increased CRC cell apoptosis.MicroRNA-145 (miR-145) was speculated as a target miRNA of LINC00662 by bioinformatics analysis. Luciferase reporter assays and RNA pull-down assays verified that LINC00662 directly interacted with miR-145. Expression of miR-145 was downregulated in CRC tissues and cell lines. Up-regulation of miR-145suppressed cell growth and promoted apoptosis in CRC cells. Suppression of miR-145markedly reversed the suppressive function of LINC00662 knockdown on CRC cell growth. In addition, c-myc was confirmed as a target gene of miR-145 in CRC cells.  Recover of c-myc expression partially reversed suppression effect mediated by LINC00662 downexpression or miR-145overexpressionon CRC cell growth. Taken together, our results indicate that LINC00662lead to the malignant behavior of CRC cells by upregulating c-myc via sponging miR-145, underlining the essential role of the LINC00662/miR-145/c-myc axis in regulating the growth of CRC cells.

The Effect of PEI-Mediated E1A on the Radiosensitivity of Hepatic Carcinoma Cells.

OBJECTIVE: The study was undertaken to investigate the effects of polyethyleneimine (PEI)-mediated adenovirus 5 early region 1A (E1A) on radiosensitivity of human hepatic carcinoma cell in vitro and to disclosure the underlying mechanism. MATERIALS AND METHODS: Human hepatic carcinoma SMMC-7721 cell line was transfected with E1A gene using PEI vector. Untransfected cells (SMMC-7721 group), cells transfected with blank-vector (SMMC-7721-vect group), and cells transfected with E1A gene (SMMC-7721-E1A group) were treated with 6 MV X-ray irradiation at doses of 0, 1, 2, 4, 8 and Gy, respectively. Radiosensitivity was determined by MTT assay and quantified by calculating the cell survival rate. Cell-cycle distribution and apotosis rate were monitored by flow cytometry. RESULTS: The survival rate of SMMC-7721-E1A was significantly lower than that of SMMC-7721 cell. Apoptosis rate of SMMC-7721-E1A group was significantly higher than that of SMMC-7721group (P<0.01).The ratio of S stage in cell cycle of SMMC-7721-E1A was significantly lower than that in SMMC-7721 cell. The ratio of G2/M stage in cell cycle of SMMC-7721-E1A was significantly higher than that in SMMC-7721 cell (P<0.01). CONCLUSION: PEI could transfect E1A gene into hepatic carcinoma cells PEI-mediated E1A could effectively enhance radiosensitivity of hepatic carcinoma cells which may be related to its effects on apoptosis promoting leading to S phase suppression and G2/M phase arrest.
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Research Progress on Long Non-Coding RNA and Radiotherapy.

d_abstr_R Long non-coding RNAs (lncRNAs), a group of non-protein-coding RNAs longer than 200 nucleotides, are involved in multiple biological and pathological processes, such as proliferation, apoptosis, migration, invasion, angiogenesis, and immune escape. Many studies have shown that lncRNAs participate in the complex network of cancer and play vital roles as oncogenes or tumor-suppressor genes in a variety of cancers. Moreover, recent research has shown that abnormal expression of lncRNAs in malignant tumor cells before and after radiotherapy may participate in the progression of cancers and affect the radiation sensitivity of malignant tumor cells mediated by specific signaling pathways or cell cycle regulation. In this review, we summarize the published studies on lncRNAs in radiotherapy regarding the biological function and mechanism of human cancers, including esophageal cancer, pancreatic cancers, nasopharyngeal carcinoma, hepatocellular carcinoma, cervical cancer, colorectal cancer, and gastric cancer.

Polyethylenimine (PEI)-Mediated E1A Increases the Sensitivity of Hepatocellular Carcinoma Cells to Chemotherapy.

BACKGROUND The aim of this study was to assess the ability of polyethylenimine (PEI) as an E1A plasmid vector to transfect hepatocellular carcinoma SMMC-7721 cells and to analyze the sensitization effect of E1A on various anti-tumor drugs. MATERIAL AND METHODS PEI-mediated recombinant plasmid psv-E1A with high expression of the E1A gene was introduced into hepatocellular carcinoma SMMC-7721 cells, and the effective transfection of E1A gene was determined by RT-PCR and Western blot analysis. The CCK8 method was used to detect the proliferation inhibition of docetaxel, epirubicin, gemcitabine, and 5-fluorouracil on SMMC-7721 cells before and after the transfection of the E1A gene. RESULTS RT-PCR and Western blot analysis showed that PEI could transfect plasmid psv-E1A with stable expression. After the transfection of E1A gene, the sensitivity of SMMC-7721 cells to docetaxel, epirubicin, gemcitabine, and 5-fluorouracil was increased (P<0.05), and the sensitivity to docetaxel was significantly improved (P<0.01). CONCLUSIONS PEI can transfect plasmid psv-E1A. The E1A gene can increase the sensitivity of hepatocellular carcinoma cells to chemotherapeutic drugs. The mechanism may be related to the increased ability of the E1A gene to inhibit proliferation of hepatocellular carcinoma cells and altering the cell cycle of hepatocellular carcinoma cells.

EGFR inhibitor C225 Increases the Radio-Sensitivity of Human Breast Cancer Cells

Objective: This study was undertaken to investigate the effect of C225 on the radio-sensitivity of MDA-MB-231 cells line and to disclosure underlying mechanism. Methods: CCK8 assay was used to measure the proliferation inhibition of C225 on MDA-MB-231 cells. The combined effects of C225 plus radiation on the proliferation of MDA-MB-231 cells were also evaluated by CCK-8 assay. The clonogenic assay was performed to evaluate the cell surviving fractions and to determine the radio-sensitizing effect of C225 on MDA-MB-231 cells. The apoptosis and cell cycle distribution were analyzed by flow cytometry. Western blot analysis was used to detect the expression of p-EGFR, p-Akt, p-P38, and caspase-3. Results: C225 had an inhibiting effect on the proliferation of cells in a concentration-dependent manner. The cloning formation capacity was decreased in C225 plus radiation group. C225 increased radio-sensitivity of cells and led to cell cycle arrest in G0/G1 phase markedly. Cells treated with C225 and radiation predominantly exhibited G0/G1 phase arrest and significant decreased in the fraction of cells in the S phase. Moreover, C225 and radiation significantly increased the apoptosis rate of cells. Decreased cell proliferation was further supported by the down-regulation of p-EGFR and its downstream singling pathway proteins such as p-Akt and p-P38. The up-regulation of the Caspase-3 expression in C225 plus radiation group revealed that C225 could increase radiation-inducing cell apoptosis. Conclusion: C225 could increase the radio-sensitivity of cells, which may be due to the anti-proliferative synergistic effect between C225 and radiation as well as the down-regulation of the PI3K/Akt signaling pathway.