RESUMO
Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the cell migration and invasion assay data shown in Figs. 2C and 5C were strikingly similar to data appearing in different form in other articles by different authors at different research institutes. Owing to the fact that the contentious data in the above article were already under consideration for publication prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 38253832, 2017; DOI: 10.3892/mmr.2017.7077].
RESUMO
BACKGROUND: Among the different types of cancer, pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC), is the most lethal malignancy, with poor early detection rates and prognosis. The aim of the present study was to investigate the potential genetic effects of the single-nucleotide polymorphisms (SNPs) in ABCB1 (rs1045642, rs3789243, rs4148737), APOB (rs693, rs1042031), CAV1 (rs12672038, rs1997623, rs3807987, rs7804372), and NAMPT (rs9034, rs2505568, rs61330082) on PDAC. METHODS: A total of 273 patients with PDAC and 263 healthy controls were genotyped using PCR and direct Sanger sequencing. Unconditional logistic regression models were used to evaluate the potential effects of the genotypes, alleles, and haplotypes on the risk of developing PDAC. RESULTS: Patients with PDAC possessed a considerably lower frequency of genotypes AG, GG, and allele G at ABCB1 rs4148737 compared with controls. Based on age, sex, smoking status, drinking status, diabetes, and family history of cancer, stratified analyses showed a significant correlation between SNPs at rs4148737 and PDAC. According to specific SNPs, eight haplotypes were constructed along with ABCB1 rs4148737, rs1045642, and rs3789243. Carriers with haplotypes ACC and ATC were more susceptible to developing PDAC, whereas haplotypes GCC and GTC were associated with a reduced likelihood of developing PDAC. The distributions of the other SNPs in each group were not significantly associated with PDAC risk. CONCLUSIONS: These results suggested that genetic polymorphisms of ABCB1 rs4148737 may influence an individual's risk of developing PDAC.
Assuntos
Apolipoproteína B-100/genética , Carcinoma Ductal Pancreático/genética , Caveolina 1/genética , Citocinas/genética , Nicotinamida Fosforribosiltransferase/genética , Neoplasias Pancreáticas/genética , Polimorfismo de Nucleotídeo Único , Subfamília B de Transportador de Cassetes de Ligação de ATP/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , China , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
Colorectal cancer (CRC) is the third most common type of diagnosed cancer and the fourth leading cause of cancerassociated mortalities worldwide. Increasing studies have demonstrated that the deregulation of microRNAs (miRNAs or miRs) is associated with the occurrence and development of multiple types of human cancer, including CRC. miR329 has been identified to be downregulated in various types of cancer; however, its expression pattern, functions and mechanisms in CRC remain unclear. The present study demonstrated that miR329 was lowly expressed in CRC tissue samples and cell lines. Low expression of miR329 was correlated with tumornodemetastasis stage and lymph node metastasis in patients with CRC. In vitro experiments revealed that resumption expression of miR329 suppressed cell proliferation and invasion in CRC. Furthermore, the results of the present study indicated that miR329 targets transforming growth factorß1 (TGFß1) directly in vitro. TGFß1 was demonstrated to be upregulated in CRC tissue samples and inversely correlated with miR329 expression. Upregulation of TGFß1 was able to partially counteract the antitumor roles of miR329 on CRC cell proliferation and invasion. The results of the current study revealed that miR329 suppresses CRC cell proliferation and invasion through targeting TGFß1, thus suggesting that targeting miR329/TGFß1 may provide a novel effective therapeutic approach for the treatment of patients with CRC.
Assuntos
Neoplasias Colorretais/patologia , MicroRNAs/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Regiões 3' não Traduzidas , Idoso , Antagomirs/metabolismo , Sequência de Bases , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Neoplasias Colorretais/metabolismo , Regulação para Baixo , Feminino , Células HCT116 , Células HT29 , Humanos , Masculino , MicroRNAs/antagonistas & inibidores , MicroRNAs/genética , Pessoa de Meia-Idade , Alinhamento de Sequência , Fator de Crescimento Transformador beta1/química , Fator de Crescimento Transformador beta1/genéticaRESUMO
The case-control study aims to investigate the association of Fas and FasL genetic polymorphisms (Fas-670A/G (rs1800682), Fas-1377G/A (rs2234767) and FasL-844T/C (rs763110)) with esophageal carcinoma susceptibility in a north Chinese population. A total of 204 patients with esophageal carcinoma and 248 healthy controls were enrolled from Henan, China and genotyped by the polymerase chain reaction and restriction fragment length polymorphism method. There were no significant differences in distributions of their genotypes frequencies between patients and controls in Fas-670A/G, Fas-1377G/A and FasL-844T/C polymorphisms (P > 0.05). Stratified analysis showed that no significant association was found between esophageal carcinoma and gene polymorphisms of Fas-670 A/G, Fas-1377G/A, and FasL-844T/C (P > 0.05). Genetic polymorphisms in the death pathway genes Fas and FasL were not associated with risk of developing esophageal carcinoma in a north Chinese population.