Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 6 de 6
Filter
1.
World J Clin Cases ; 9(26): 7901-7908, 2021 Sep 16.
Article in English | MEDLINE | ID: mdl-34621844

ABSTRACT

BACKGROUND: Colorectal mucinous adenocarcinoma is a distinct subtype of colorectal adenocarcinoma that is not sensitive to chemotherapy and radiotherapy, and its prognosis is worse than that of nonmucinous adenocarcinoma. Early diagnosis and aggressive surgical treatment may be the key to improving the prognosis of patients. Ascending colon mucinous adenocarcinoma with the primary manifestation of a local abscess caused by non-intestinal perforation has never been reported. Moreover, since the lumen of the ascending colon is large, and early stage ascending colon cancer lacks typical clinical manifestations, the diagnosis may be delayed easily. We herein report three cases of delayed diagnosis of colorectal mucinous adenocarcinoma. CASE SUMMARY: We present three patients (two females and one male) with mucinous ascending colon mucinous adenocarcinoma with the primary manifestation of a local abscess (the right area of the lumbar spine, right groin, and lower right abdomen) caused by non-intestinal perforation. At the initial clinical visit, the common causes of those abscesses, including spinal tuberculosis and urinary tract infection, were excluded. The treatment of the abscess was through an incision and drainage. However, the source of the abscess was not made clear, which led to an abscess recurrence and a delayed diagnosis of colorectal mucinous adenocarcinoma. After the patients were referred to our hospital, a definitive diagnosis of ascending colon mucinous adenocarcinoma was made with the help of tumor markers and colonoscopic findings. Because of the delayed diagnosis of the disease, two patients (case 1 and case 2) missed the chance of surgery due to disease progression and died in a short follow-up period. Only case 3 underwent radical surgery for the tumor in the right colon and partial abdominal wall resection and achieved a better prognosis. CONCLUSION: Abscesses in the right area of the lumbar spine, right groin, or right lower quadrant caused by non-intestinal perforation as the primary clinical manifestation of ascending colon mucinous adenocarcinoma are extremely rare. Mucinous adenocarcinoma of the ascending colon may be one of the causes of such abscesses. Performing colonoscopy as soon as possible is of great significance in the diagnosis and treatment of the disease.

2.
Oncol Rep ; 46(4)2021 10.
Article in English | MEDLINE | ID: mdl-34396427

ABSTRACT

The presence of cancer stem cells (CSCs) is a major cause of therapeutic failure in a variety of cancer types, including colorectal cancer (CRC). However, the underlying mechanisms that regulate the self­renewal of colorectal cancer stem cells (CRCSCs) remain unclear. Our previous study utilized CRCSCs and their parent cells; through gene microarray screening and bioinformatics analysis, we hypothesized that microRNA (miR)­8063 may bind to, and regulate the expression of, heterogeneous nuclear ribonucleoprotein AB (hnRNPAB) to facilitate the regulation of CRCSC self­renewal. The aim of the present study was to confirm this conjecture through relevant experiments. The results indicated that compared with that in parent cells, miR­8063 expression was significantly downregulated in CRCSCs, while hnRNPAB expression was increased. Furthermore, hnRNPAB was identified as a direct target of miR­8063 using a dual­Luciferase assay. Overexpression of hnRNPAB promoted the acquisition of CSC characteristics in CRC cells (increased colony formation ability, enhanced tumorigenicity, and upregulated expression of CSC markers), as well as the upregulation of key proteins (Wnt3a, Wnt5a and ß­catenin) in the Wnt/ß­catenin signaling pathway. Similarly, after silencing miR­8063 in CRC cells, the characteristics of CSC were altered, and the expression of hnRNPAB protein was promoted. However, post overexpression of miR­8063 in CRCSCs, the self­renewal ability of CSCs was weakened with the downregulation of hnRNPAB protein, Wnt3a, Wnt5a and ß­catenin. These results suggest that as a tumor suppressor, miR­8063 is involved in regulating the self­renewal of CRCSCs, where loss of miR­8063 expression weakens its inhibition on hnRNPAB, which leads to the activation of Wnt/ß­catenin signaling to promote the self­renewal of CRCSCs.


Subject(s)
Colorectal Neoplasms/genetics , Heterogeneous-Nuclear Ribonucleoproteins/genetics , MicroRNAs/genetics , Neoplastic Stem Cells/metabolism , Wnt Signaling Pathway/genetics , beta Catenin/genetics , Colorectal Neoplasms/metabolism , Down-Regulation , HT29 Cells , Heterogeneous-Nuclear Ribonucleoproteins/metabolism , Humans , MicroRNAs/metabolism , Up-Regulation , beta Catenin/metabolism
3.
Oncol Lett ; 18(6): 6459-6468, 2019 Dec.
Article in English | MEDLINE | ID: mdl-31819776

ABSTRACT

Heterogeneous ribonucleoprotein AB (hnRNP AB) is a member of the heterogeneous nuclear ribonucleoprotein family, which serves important functions in gene expression and signal transduction. However, the expression and clinicopathological significance of hnRNP AB in colorectal cancer (CRC) remain to be elucidated. To investigate the expression and clinical significance of hnRNP AB in CRC, hnRNP AB expression levels were analysed in two independent cohorts of patients with CRC. The results of reverse transcription-quantitative PCR, immunohistochemistry and western blot analysis demonstrated that hnRNP AB was upregulated in CRC tissues compared with the corresponding adjacent normal tissues. Immunohistochemical analyses indicated that a high expression of hnRNP AB was significantly associated with preoperative carcinoembryonic antigen (CEA; P<0.001) and carbohydrate antigen 19-9 (P=0.014) levels, tumour size (P=0.022) and infiltration (P=0.026), lymph node metastasis (P<0.001) and Tumour-Node-Metastasis stage (P<0.001). Univariate and multivariate Cox survival analyses revealed that hnRNP AB expression and preoperative CEA levels were significant independent factors affecting overall survival in patients with CRC (P<0.05). According to the Kaplan-Meier model, patients with CRC with high hnRNP AB expression exhibited significantly poorer prognosis compared with those with low hnRNP AB expression (P<0.001). In conclusion, the results of the present study demonstrated that hnRNP AB expression may serve an important role in the progression of CRC and that hnRNP AB may be considered a predictor of prognosis for patients with CRC.

4.
Mol Ther Oncolytics ; 15: 7-20, 2019 Dec 20.
Article in English | MEDLINE | ID: mdl-31650021

ABSTRACT

Cancer stem cells (CSCs) are the main cause of tumor generation, recurrence, metastasis, and therapy failure in various malignancies including colorectal cancer (CRC). Accumulating evidence suggests that tumor cells can acquire CSC characteristics through the epithelial-mesenchymal transition (EMT) process. However, the molecular mechanism of CSCs remains unclear. OCT4B1 is a transcript of OCT4, which is initially expressed in embryonic stem and carcinoma cells, and is involved in the regulation and maintenance of an undifferentiated state of stem cells. In this study, three-dimensional (3D) microspheres were confirmed as CRC stem cells. Compared with that of parental cells, their self-renewal ability was significantly increased, and OCT4B1 expression was increased and promoted the EMT process. The knockdown of OCT4B1 decreased the self-renewal of CSCs and reversed EMT. Moreover, OCT4B1 induced the expression of Polo-like kinase 1 (PLK1), which is a key regulator of EMT in tumor cells. Further examination showed that OCT4B1 regulated the miR-8064/PLK1 balance to exert its function. Taken together, our data suggest that OCT4B1 may be involved in regulating the self-renewal of colorectal CSCs through EMT, which is at least partially due to the miR-8064/PLK1 balance. This study indicates that OCT4B1 is a potential therapeutic target for CRC by targeting CSCs.

5.
Oncol Rep ; 34(6): 2943-52, 2015 Dec.
Article in English | MEDLINE | ID: mdl-26398480

ABSTRACT

OCT4B1, a splice variant of OCT4, is a key regulator in maintaining the properties of pluripotency and self-renewal in embryonic stem (ES) cells. Recent results have shown that OCT4B1 is involved in tumorigenesis. However, the contribution of OCT4B1 in the tumorigenesis and drug resistance of colon cancer remains to be determined. The aim of the present study was to determine whether OCT4B1, which maintains the stemness of ES cells, promoted cell growth by facilitating transition of the cell cycle and reduced apoptosis in colon cancer and drug­resistant cells using flow cytometry and western blotting. The results showed that, OCT4B1 promoted the growth of colon cancer and drug­resistant cancer cells by maintaining the activity of ES cells and by facilitating the transition of the cell cycle and reducing apoptosis. Additionally, OCT4B1 was able to reduce sensitivity to oxaliplatin by altering the expression of two important mediators in drug resistance, P-gp and ABCG2 [ATP-binding cassette, sub­family G (WHITE), member 2]. Furthermore, OCT4B1 enhanced the ability of migration and invasion through alteration of the epithelial-to-mesenchymal transition (EMT) in colon cancer. In conclusion, to the best of our knowledge, the results demonstrated for the first time that OCT4B1 functions as an oncogene in colon cancer and provides the development of novel therapeutic strategies to treat colon cancer, particularly drug resistance.


Subject(s)
Carcinogenesis/genetics , Colonic Neoplasms/genetics , Drug Resistance, Neoplasm/genetics , Octamer Transcription Factor-3/genetics , ATP Binding Cassette Transporter, Subfamily B, Member 1/biosynthesis , ATP Binding Cassette Transporter, Subfamily G, Member 2 , ATP-Binding Cassette Transporters/biosynthesis , Apoptosis , Cell Cycle/genetics , Cell Movement/genetics , Cell Proliferation/genetics , Colonic Neoplasms/drug therapy , Colonic Neoplasms/pathology , Embryonic Stem Cells/pathology , Epithelial-Mesenchymal Transition/genetics , Humans , Neoplasm Invasiveness/genetics , Neoplasm Invasiveness/pathology , Neoplasm Proteins/biosynthesis , Octamer Transcription Factor-3/biosynthesis
6.
Clin Res Hepatol Gastroenterol ; 37(6): 602-7, 2013 Dec.
Article in English | MEDLINE | ID: mdl-24012221

ABSTRACT

Hepatic fibrosis is a major consequence of liver aggression. Finding novel ways for counteracting this damaging process, and for evaluating fibrosis with a non-invasive imaging approach, represent important therapeutic and diagnostic challenges. Hepatocyte growth factor (HGF) is an anti-fibrosis cell growth factor that induces apoptosis in activated hepatic stellate cells, reduces excessive collagen deposition, and stimulates hepatocyte regeneration. Thus, using HGF in gene therapy against liver fibrosis is an attractive approach. The aims of the present study were: (i) to explore the efficacy of treating liver fibrosis using HGF expression vector carried by a novel ultrasound microbubble delivery system; (ii) to explore the diagnostic interest of diffusion-weighted MRI (DWI-MRI) in evaluating liver fibrosis. We established a rat model of hepatic fibrosis. The rats were administered HGF linked to novel ultrasound micro-bubbles. Progression of hepatic fibrosis was evaluated by histopathology, hydroxyproline content, and DWI-MRI to determine the apparent diffusion coefficient (ADC). Our targeted gene therapy produced a significant anti-fibrosis effect, as shown by liver histology and significant reduction of hydroxyproline content. Moreover, using DWI-MRI, the b value (diffusion gradient factor) was equal to 300s/mm(2), and the ADC values significantly decreased as the severity of hepatic fibrosis increased. Using this methodology, F0-F2 could be distinguished from F3 and F4 (P<0.01). This is the first in vivo report of using an ultrasound microbubble-cationic nano-liposome complex for gene delivery. The data indicate that, this approach is efficient to counteract the fibrosis process. DWI-MRI appears a promising imaging technique for evaluating liver fibrosis.


Subject(s)
Diffusion Magnetic Resonance Imaging , Gene Transfer Techniques , Hepatocyte Growth Factor/administration & dosage , Liver Cirrhosis/pathology , Liver Cirrhosis/therapy , Microbubbles , Animals , Common Bile Duct/injuries , Disease Models, Animal , Drug Carriers , Echo-Planar Imaging , Genetic Therapy , Hepatocyte Growth Factor/genetics , Hydroxyproline/metabolism , Ligation , Liposomes/chemistry , Liver/diagnostic imaging , Liver/metabolism , Liver/pathology , Liver Cirrhosis/metabolism , Male , Nanoparticles/chemistry , Phosphatidylethanolamines , Polyethylene Glycols , Rats , Rats, Sprague-Dawley , Severity of Illness Index , Sonication/methods , Ultrasonography
SELECTION OF CITATIONS
SEARCH DETAIL
...