Effect of human chorionic gonadotropin in the gene expression profile of MCF-7 cells
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The preventive effect of human chorionic gonadotropin (hCG)-induced differentiation on experimental mammary carcinogenesis has been reported to be due to the inhibition of cell proliferation, increased DNA repair capabilities of the mammary epithelium, decreased binding of the carcinogen to the DNA and activation of programmed cell death genes leading to apoptosis. To further our understanding of the molecular pathway of the hCG action on mammary epithelial cells we have analyzed gene expression profiles of MCF-7 cells treated with hCG for 24, 48, and 96 h, using a DNA microarray consisting of 1176 genes. Comparison of expression between the treated and not treated cells enabled us to identify 48 genes that are affected by this hormone. Importantly, there is a cluster of genes that are overexpressed during the first 24 h and level off thereafter, whereas other genes are maximally expressed at 96 h of treatment. The results obtained in this study demonstrated that genes regulating cell proliferation, apoptosis, cell trafficking, and DNA repair are significantly affected by hCG in human breast cancer cells in vitro.Keywords:
Human chorionic gonadotropin
The authors of the above article drew to our attention that they had identified three instances of data overlapping between data panels, suggesting that data purportedly showing results obtained under different experimental conditions had been derived from the same original source. Comparing between the two figures, two pairs of panels in Fig. 4B (the Mimics control and blank experiments for the U87 and U251 cell lines) were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B (the data panels for the miR‑375 mi + .pCDNA/RWDD3 and miR‑375 mi + .pCDNA experiments for the U87 cell line). The authors were able to re‑examine the original data files and retrieve the correct data panels. The errors in these figures arose through inadvertently assembling Figs. 4 and 6 incorrectly. The revised versions of Figs. 4 and 6, featuring the corrected data panels for the Mimics control and blank experiments for the U87 and U251 cell lines in Fig. 4B, and the correct data for the U87 cell line in Fig. 6B, are shown opposite and on the next page, respectively. Note that the corrections to the data shown in these Figures do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 39: 1825-1834, 2018; DOI: 10.3892/or.2018.6261].
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Radiotherapy is an important therapeutic strategy for the treatment of numerous types of malignant tumors, including glioma. However, radioresistance and anti‑apoptotic mechanisms decrease the efficacy of radiotherapy in many patients with glioma. BMI1 polycomb ring finger oncogene (Bmi‑1) is an oncogene associated with radioresistance in tumor cells. MicroRNA (miRNA)‑128a is a brain-specific miRNA, which suppresses Bmi‑1 expression. The present study investigated the effects of various radiation intensities on U‑87 MG glioma cells, as well as the role of reactive oxygen species (ROS), Bmi‑1, and miRNA‑128a in the cellular response to radiotherapy. The response of U‑87 MG cells following exposure to X‑ray radiation was assessed using a cell growth curve and inhibition ratio. Cell cycle distribution and the levels of intracellular ROS were evaluated by flow cytometry. The mRNA expression levels of Bmi‑1 and those of miRNA‑128a in U‑87 MG cells exposed to X‑ray radiation were evaluated by reverse transcription‑quantitative polymerase chain reaction. X‑ray radiation did not decrease the number of U‑87 MG cells; however, it did inhibit cellular growth in a dose‑dependent manner. Following exposure to X‑ray radiation for 24 h, cell cycle distribution was altered, with an increase in the number of cells in G0/G1 phase. The mRNA expression levels of Bmi‑1 were downregulated in the 1 and 2 Gy groups, and upregulated in the 6 and 8 Gy groups. The expression levels of miRNA‑128a were upregulated in the 1 and 2 Gy groups, and downregulated in the 8 Gy group. The levels of ROS were increased following exposure to ≥2 Gy, and treatment with N-acetyl cysteine was able to induce radioresistance. These results suggested that U‑87 MG cells exhibited radioresistance. High doses of X‑ray radiation increased the expression levels of Bmi‑1, which may be associated with the evasion of cellular senescence. miRNA‑128a and its downstream target gene Bmi‑1 may have an important role in the radioresistance of U‑87 MG glioma cells. In addition, ROS may be involved in the mechanisms underlying the inhibitory effects of X‑ray radiation in U‑87 MG cells, and the downregulation of ROS may induce radioresistance.
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Kidney cancer is the 14th most common cancer in the world and its prognosis remains poor due to difficult early detection and treatment. Therefore, the identification of biomarkers for early‑stage renal cell carcinoma (RCC) is important. MicroRNA‑106b (miR‑106b) has been described as an oncogene in several types of human cancer. Previous microarray studies have suggested that miR‑106b was significantly upregulated in RCC tissues compared with paired normal kidney tissues and may be a promising biomarker for the prediction of early metastasis following nephrectomy. The present study aimed to determine the expression and function of miR‑106b in RCC. The expression of miR‑106b in RCC tissues and cells, and in paired normal tissues and cells was determined by reverse transcription quantitative polymerase chain reaction, based on the previous sequencing results of miRNAs. Furthermore, a wound scratch assay, MTT assay and flow cytometry were performed to examine the functions of miR‑106b on cell migration, proliferation and apoptosis. The results demonstrated that miR‑106b was upregulated in RCC tissues and cell lines compared with control normal tissues and cell lines. Downregulation of miR‑106b with a synthesized inhibitor suppressed cell migration and proliferation and induced renal cancer cell apoptosis, suggesting that miR‑106b can be characterized as an oncogene in RCC. To the best of our knowledge, the present study was the first to reveal that miR‑106b is upregulated and affects cellular migration, proliferation and apoptosis in RCC. Further studies are required to examine the role and target genes of miR‑106b in RCC.
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This study aimed to determine whether manipulation of the microRNA‑200 (miR‑200) family could influence colon adenocarcinoma cell behavior. The miR‑200 family has a significant role in tumor suppression and functions as an oncogene. In vitro studies on gain and loss of function with small interfering RNA demonstrated that the miR‑200 family could regulate RASSF2 expression. Knockdown of the miR‑200 family in the HT‑29 colon cancer cell line increased KRAS expression but decreased signaling in the MAPK/ERK signaling pathway through reduced ERK phosphorylation. Increased expression of the miR‑200 family in the CCD‑841 colon epithelium cell line increased KRAS expression and led to increased signaling in the MAPK/ERK signaling pathway but increased ERK phosphorylation. Functionally, knockdown of the miR‑200 family led to decreased cell proliferation in the HT‑29 cells; therefore, increased miR‑200 family expression could increase cell proliferation in the CCD‑841 cell line. The present study included a large paired miR array dataset (n=632), in which the miR‑200 family was significantly found to be increased in colon cancer when compared with normal adjacent colon epithelium. In a miR‑seq dataset (n=199), the study found that miR‑200 family expression was increased in localized colon cancer compared with metastatic disease. Decreased expression was associated with poorer overall survival. The miR‑200 family directly targeted RASSF2 and was inversely correlated with RASSF2 expression (n=199, all P<0.001). Despite the well‑defined role of the miR‑200 family in tumor suppression, the present findings demonstrated a novel function of the miR‑200 family in tumor proliferation.
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B7 homolog 6 (B7‑H6) was recently discovered to act as a co‑stimulatory molecule. In particular, the expression of B7‑H6 has been found to play an important biological role in several types of tumors. The aim of the present study was to determine the role of B7‑H6 in cervical cancer. Immunohistochemistry was used to analyze the expression levels of B7‑H6 in cervical precancerous and cancerous tissues. Furthermore, the expression of B7‑H6 was knocked down in HeLa cells using short hairpin RNA and the effects of B7‑H6 on HeLa cell proliferation, migration and invasion were determined using Cell Counting Kit‑8, colony formation, wound healing and Transwell invasion assays, respectively. In addition, flow cytometry was used to analyze the levels of cell apoptosis and the cell cycle distribution. The results of the immunohistochemical staining revealed that the expression levels of B7‑H6 were upregulated in cervical lesions. Furthermore, the expression levels of B7‑H6 were positively associated with the clinical stage of the cervical lesions. B7‑H6 knockdown suppressed the invasive, migratory and proliferative abilities of HeLa cells, and promoted G1 cell cycle arrest and apoptosis. In conclusion, the findings of the present study suggested that B7‑H6 may serve as a novel oncogene and may hold promise as a potential therapeutic target for cervical cancer.
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The analysis of oncogene expression may provide insights into the pathogenesis of small cell lung cancer (SCLC) and may help to predict clinical behavior. The expression of 8 oncogenes (c-myc, N-myc, L-myc, Ha-ras, Ki-ras, N-ras, erbB-2, v-sis) was evaluated in small cell lung cancer (SCLC) xenografts of tumor samples, recentlly transplanted, taken from 17 different patients. Eight of these 17 SCLC lines expressed the L-myc oncogene and 2 SCLC lines expressed the c-myc oncogene. One SCLC line (SCLC-63M) simultaneously expressed the L-myc and c-myc oncogenes. All SCLC lines examined had almost similar high RNA levels of the Ki-ras oncogene, while the expression of Ha- and N-ras oncogenes was not always observed. The N-myc and v-sis oncogenes were expressed in only one tumor and at a very weak level, and no transcript of the erbB-2 oncogene was observed in any of our 17 SCLC lines. These results indicate that oncogene expression in SCLC lines is heterogeneous, with the exception of the Ki-ras oncogene which is constantly overexpressed.
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