RESUMO
The current work was intended to explore the function and mechanism of Kinesin family member 2C (KIF2C) in hepatocellular carcinoma (HCC). In this study, KIF2C expression was at a high level in HCC and indicated poor prognosis. Silencing KIF2C significantly suppressed the proliferation, migration, and invasion in HCC cells. Furthermore, silencing KIF2C markedly decreased the expression of Snail, Vimentin, p-MEK, and p-ERK, but increased E-cadherin expression in HCC cells. Moreover, we also found that MEK/ERK inhibitor U0126 could enhance the impact on cell proliferation, migration, and invasion induced by silencing KIF2C in HCC. On the contrary, MEK/ERK activator PAF could weaken the impact induced by silencing KIF2C in HCC. Thus, our findings indicate that KIF2C can promote the proliferation, migration, and invasion by activating MEK/ERK pathway in HCC.
Assuntos
Carcinoma HepatocelularRESUMO
The present study aimed to explore the regulatory mechanism of long intergenic nonprotein coding (LINC)00238 in hepatocellular carcinoma (HCC). LINC00238 expression in HCC tissues and cell lines was measured using reverse transcriptionquantitative PCR. LncTar was used to predict the binding sites between LINC00238 and transmembrane protein 106C (TMEM106C). Survival analysis of LINC00238, TMEM106C and activating transcription factor 3 (ATF3) in patients with HCC was performed based on TCGA data. The proliferation, apoptosis, migration, and invasion of HCC cells were measured by 3(4,5dimethylthiazol2yl)5(3carboxymethoxyphenyl)2(4sulfophenyl)2Htetrazolium assay, ï¬ow cytometer, wound healing and Transwell assays, respectively. LINC00238 promoted apoptosis and inhibited proliferation, migration and invasion of HCC cells. LINC00238 was downregulated in HCC. TMEM106C was a target of LINC00238 and TMEM106C expression was negatively regulated by LINC00238. TMEM106C suppressed the apoptosis pathway and decreased the expression of caspase7, tissue inhibitor of metalloproteinase 2, programmed cell death 4 and ATF3. Notably, ATF3 was the upstream promoter of LINC00238 and positively regulated LINC00238 expression. In conclusion, LINC00238 inhibited HCC progression by inhibiting TMEM106 expression and activating the TMEM106Cmediated apoptosis pathway.
Assuntos
Fator 3 Ativador da Transcrição/metabolismo , Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , Proteínas de Membrana/genética , RNA Longo não Codificante/metabolismo , Adulto , Idoso , Apoptose/genética , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/cirurgia , Linhagem Celular Tumoral , Conjuntos de Dados como Assunto , Regulação para Baixo , Retroalimentação Fisiológica , Feminino , Regulação Neoplásica da Expressão Gênica , Hepatectomia , Humanos , Fígado/patologia , Fígado/cirurgia , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/cirurgia , Masculino , Proteínas de Membrana/metabolismo , Pessoa de Meia-Idade , Regiões Promotoras Genéticas/genética , RNA Longo não Codificante/genética , Transdução de Sinais/genéticaRESUMO
Amine oxidase copper containing 1 (AOC1) is a copper-containing amine oxidase that catalyzes the deamination of polyamines. AOC1 functions as an oncogene in human gastric cancer. There is little information available regarding the function of AOC1 in hepatocellular carcinoma (HCC). In the present study, reverse transcription-quantitative PCR was used to detect the expression levels of AOC1 in HCC tissues, and the role of AOC1 in HCC progression was determined using western blot, Cell Counting Kit 8, clone formation, wound-healing and Transwell assays. An AOC1 survival curve was generated with data downloaded from The Cancer Genome Atlas, and Gene Set Enrichment Analysis was performed to investigate the potential biological mechanisms of AOC1 in HCC. AOC1 was found to be upregulated in HCC tissues, which was associated with a poor prognosis. Furthermore, AOC1-knockdown inhibited HCC cell proliferation, migration and invasiveness, suppressed IL-6 expression, as well as decreasing JAK2 and STAT3 phosphorylation. Ultimately, the results of the present study illustrate that AOC1 promoted the proliferation, migration and invasiveness of HCC cells by regulating the IL-6/JAK/STAT3 pathway.
RESUMO
OBJECTIVE: To evaluate the application of mycobacterial interspersed repetitive units (MIRU) in typing Mycobacterium tuberculosis in Shandong. METHOD: 826 strains of M. tuberculosis from laboratories of 12 county tuberculosis dispensaries in Shandong were cultured and typed by MIRU genotyping in the KICID laboratory. RESULTS: The 826 strains were typed to 201 distinct MIRU patterns, and 123 isolates were unique, 703 strains were grouped into 1 of 78 different MIRU clusters, and the MIRU genotype of the largest cluster was 223325173533. Among the clustered strains, 18 patients had an epidemiological history of contact. The Hunter-Gaston discriminatory index was 0.90. The allelic diversity of the sample was calculated for each other of the MIRU loci, and showed that MIRU26 had 10 alleles and was highly discriminative, while other five MIRU loci (MIRU31, 10, 39, 40, 4) were moderately discriminative. The reproducibility of the MIRU method was 100%. It took about RMB yen50 to genotype one strain. CONCLUSIONS: MIRU genotyping is a reproducible, fast, simple, and relatively cheap method. But because the isolates of 223325173533 genotype are predominant (30.89% of the isolates) in Shandong Province, it needs a second method IS6110 RFLP or by adding other more discriminative variable-number tandem repeat (VNTR) loci to improve the discriminative power.