RESUMO
Gallbladder neuroendocrine carcinoma (GB-NEC) is a rare, aggressive neuroendocrine carcinoma that arises from the gallbladder. Patients with GB-NEC usually have a poor prognosis. The present study described two cases diagnosed with GB-NEC and reviewed the literature to improve knowledge of GB-NEC. The present study reported on two cases of GB-NEC in male patients aged 65 and 66 years, respectively. Both patients underwent surgical resection. Postoperative pathology confirmed that one case had mixed adeno-neuroendocrine carcinoma and the other had large cell neuroendocrine carcinoma. In addition, both patients had uneventful recoveries following surgery and received cisplatin-etoposide combination chemotherapy. The present study summarized the two cases and reviewed the literature to improve understanding of GB-NEC. The results revealed that radiological findings of GB-NEC are non-specific. The present study demonstrated that surgical resection was still the most effective therapy and that postoperative adjuvant chemotherapy could markedly improve the prognosis of patients with GB-NEC.
RESUMO
Chemotherapy resistance poses a major challenge for the clinical treatment of colorectal cancer, therefore, the aim of the present study was to examine its underlying mechanisms. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to determine the microRNA (miRNA)/mRNA and protein expression levels, respectively. A dual luciferase assay was conducted for verification of the interaction between miR-106a and 3'untranslated region (UTR) of Forkhead box Q1 (FOXQ1). Cell viability was assessed using an MTT assay. In the present study, it was demonstrated that miR-106a is involved in regulating oxaliplatin sensitivity of colorectal cancer. Transfection of miR-106a mimics slightly inhibited colorectal cancer cell growth and sensitized colorectal cancer cells to oxaliplatin exposure. In addition, miR-106a overexpression induced a decrease of FOXQ1 at mRNA and protein levels in colorectal cancer cells. The enhanced expression of miR-106a also increased the expression of Wnt target genes, including vascular endothelial growth factor-A and matrix metallopeptidase 2, which were reported to be regulated by FOXQ1. It was predicted and validated that miR-106a could repress FOXQ1 expression via direct binding to 3'UTR. Elevation of miR-106a and a decrease of FOXQ1 expression levels were detected in tumor tissues from patients with oxaliplatin-sensitive colorectal cancer, compared with patients with oxaliplatin-resistant colorectal cancer. Furthermore, there was a significant association between miR-106a and FOXQ1 mRNA levels. In conclusion, the present study demonstrated that miR-106a increased oxaliplatin sensitivity of colorectal cancer cells through direct repression of FOXQ1 expression.
RESUMO
Background: Kinesin Family Member 3B (KIF3B) is one of the most ubiquitously expressed KIFs, which is related to numerous physiological responses. KIF3B has also been implicated in carcinogenesis such as in hepatocellular carcinoma cells. However, the expression of KIF3B has not been studied in pancreatic cancer along with its clinical significance. Methods: Immunohistochemical assays were performed to detect the expression levels of KIF3B in the tumor tissues and adjacent non-tumor tissues. Patients were sequentially divided into different expression levels of KIF3B group based on the staining intensity of FKIF3B in tumor tissues. The link between KIF3B expression and clinical characteristics were investigated, and the role of KIF3B on pancreatic cancer cell proliferation was detected by colony formation and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, respectively. And the proliferation related proteins such as Ki67 and proliferating cell nuclear antigen (PCNA) were detected by Western blot. The possible effects of KIF3B on tumor growth were assessed in vivo. Results: KIF3B was highly expressed in human pancreatic cancer tissues. We also found KIF3B was significantly associated to the pTNM stage (*p = 0.018), lymph node metastasis (*p = 0.040) and vascular invasion (*p = 0.034). We reported that increased expression of KIF3B was significantly correlated with poor clinical outcome in our clinical cohort of pancreatic cancer. Furthermore, functional assays revealed that knockdown KIF3B in vitro and in vivo might inhibit cancer cells proliferation by affecting Ki67 and PCNA. Conclusions: Our data suggested that KIF3B was associated with pancreatic cancer malignant progression especially proliferation. Hence, KIF3B might serve as a potential therapy target of pancreatic cancer in clinical treatment.
Assuntos
Biomarcadores Tumorais/metabolismo , Carcinoma Ductal Pancreático/secundário , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , Cinesinas/metabolismo , Neoplasias Pancreáticas/patologia , Idoso , Animais , Apoptose , Biomarcadores Tumorais/genética , Carcinoma Ductal Pancreático/genética , Carcinoma Ductal Pancreático/metabolismo , Feminino , Humanos , Cinesinas/genética , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/metabolismo , Prognóstico , Taxa de Sobrevida , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
In recent years it was found that the synthesis and biological activity of ribosomes are closely associated with tumor cell growth, tumorigenesis, and malignant transformation. However, the role of regulator of ribosome synthesis 1 (RRS1) in hepatocellular carcinoma (HCC) has not yet been reported. In the present study, we aimed to examine the potential role of RRS1 in tumor cell growth by using a lentivirus-mediated RNA interference (RNAi) system in the HCC cell line SMMC-7721 in vitro. Compared with that of the negative control group (Lv-shCon), the mRNA and protein expression levels of RRS1 in SMMC-7721 cells transfected with Lv-shRRS1 were significantly decreased. Further experiments found that silencing of RRS1 gene expression in SMMC-7721 cells significantly suppressed cell proliferation, inhibited colony formation capacity, increased apoptosis and arrested cells in the G1 phase. These results suggest that the RRS1 gene plays a critical role in cell proliferation, colony formation, cell apoptosis and cell cycle distribution in human HCC cells, and that silencing of RRS1 by RNAi is a promising therapeutic approach for the treatment of HCC, and should be further developed.
Assuntos
Carcinoma Hepatocelular/genética , Proliferação de Células/genética , Neoplasias Hepáticas/genética , Proteínas Nucleares/genética , Apoptose/genética , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Feminino , Regulação Neoplásica da Expressão Gênica/genética , Técnicas de Silenciamento de Genes , Humanos , Lentivirus/genética , Neoplasias Hepáticas/patologia , Masculino , Proteínas Nucleares/antagonistas & inibidores , Interferência de RNA , RNA Mensageiro/genética , Proteínas de Ligação a RNARESUMO
Organ transplantation is very similar to the parasitism, the immune responses to the allograft and parasite share some general characters in acute stage. But host-parasite interplay seems harmonious and clinically asymptomatic carriers act as long-term reservoirs for transmission even several decades. It is proposed that the allograft also can survive long-term like the parasite harmonious with the host if we exploit the mechanism of the parasitism. How can the parasite escape the immunologic cleaning? Recent research found that: (1) Almost all the parasites infection can break the balance of Th1/Th2 and induce the Th2 bias. The level of cytokine excreted by Th2 is increased. (2) Parasite infection can interfere in antigen presentation processing through cystatins and "dendritic cell paralysis". (3) Regulatory T cells were found surrounding the local site of parasite worms. (4) Parasite infections can switch of eicosanoid metabolism, and the anti-inflammatory mediator of the plasma is increasingly manifest in the chronic infection stage. And in animal model, chronic infection can prolong the allograft survival. If the hypotheses are correct, it will give another novel therapeutic option for patients with organ transplantation.