Pathology of circulating tumor cells and the available capture tools (Review)
Yibing GuanFangshi XuJuanhua TianHongwei ChenChuance YangShanlong HuangKe GaoZiyan WanMingrui LiMinxin HeTie Chong
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Circulating tumor cell
Circulating tumor cell
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The aim of this study was to explore the effect of a traditional Chinese medicine (Xiaochaihu Tang, XCHT) on the expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 in rats with endometriosis (EMs). A total of 48 specific-pathogen-free (SPF) female Sprague-Dawley (SD) rats were randomly divided into control (n=8) and EMs (n=40) groups. The EMs model was established using a surgical procedure. At 21 days, the rats with EMs were screened and divided into four subgroups (n=8): the model control, low-dose (7.5 g/kg) XCHT-treated, high-dose (15 g/kg) XCHT-treated and gestrinone-treated (0.5 mg/kg) groups. Following 21 days of treatment, the rats were sacrificed. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to examine the mRNA and protein levels of MMP-2 and MMP-9 in the endometrium. The expression levels of MMP-2 and MMP-9 were significantly increased in the rats with EMs compared with those in normal rats. Moreover, XCHT was able to significantly inhibit the expression of MMP-2 and MMP-9 compared with that in the model control group. In conclusion, XCHT was able to decrease the expression of MMP-2 and MMP-9 in the ectopic endometrium. The present results may provide a potential theoretical basis for the therapy of EMs.
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The expression of microRNA-203 (miR-203) in esophageal squamous cell carcinoma (ESCC) tissues is remarkably lower than that in non‑ESCC tissues. We investigated how miR-203 could influence the development of ESCC cells. Our analyses revealed that miR-203 inhibited the migration and invasion of ESCC cells. Genome-wide gene expression data and target site inhibition assays showed that miR-203 appears to directly regulate LIM and SH3 protein 1 (LASP1). The knockdown of LASP1 resulted in inhibition of the migration and invasion of ESCC cells. Our results suggest that miR-203 and its target LASP1, may be associated with the progression of ESCC. In clinical ESCC specimens, the expression levels of miR-203, which were lower compared to those in normal tissues, were inversely correlated with the mRNA expression levels of LASP1. Moreover, we found that there was a significant correlation between the expression levels of miR-203 and the relapse‑free survival. The identification of a cancer network regulated by miR-203 could provide new insights into the potential mechanisms of the progression of ESCC.
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The study intended to investigate the expression levels of micro ribonucleic acid (miR)‑205 and miR‑506 in colon cancer tissues and their relationships with clinicopathological features. The expression levels of miR‑205 and miR‑506 in colon cancer tissues and para‑carcinoma normal colonic mucosa tissues were detected via fluorescence reverse transcription quantitative polymerase chain reaction (RT‑qPCR), and the expression levels of the two miRNAs in plasma of colon cancer patients and healthy control population were also detected. Moreover, the relationships of the two miRNAs with clinicopathological features of patients with colon cancer were analyzed. The expression levels of the two miRNAs in colon cancer tissues were higher than those in para‑carcinoma normal colonic mucosa tissues, and also significantly higher in plasma of the colon cancer patients than those in the healthy control population. The differences were statistically significant (P<0.05). The expression level of miR‑205 was associated with tumor‑node‑metastasis (TNM) staging and lymph node metastasis, while the expression level of miR‑506 was associated with lymph node metastasis. The differences were statistically significant (P<0.05). The expression levels of miR‑205 in the colon cancer tissues and plasma in patients had no significant correlation (r=0.467, P=0.081). There was a positive correlation between the expression levels of miR‑506 in the colon cancer tissues and plasma in patients (r=0.599, P=0.038). The expression levels of miR‑205 and miR‑506 are upregulated in the colon cancer patients, both of which may be closely related to the occurrence and development of colon cancer, and may become potential tumor markers as well as relevant therapeutic targets.
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Expression of RUNX3 gene and miR-363 in colorectal cancer was studied to explore its relationship with clinicopathological characteristics of colorectal cancer and to analyze the value of RUNX3 combined with miR-363 in the diagnosis of colorectal cancer. In total, 85 patients diagnosed with colorectal cancer in the First Peoples Hospital of Xiaoshan Hangzhou from March 2014 to July 2016 were the experiment group. Seventy healthy individuals who underwent physical examination were the control group. RT-qPCR was used to detect the expression levels of RUNX3 gene and miR-363 in peripheral blood of the two groups. The relationship between the expression of RUNX3 and miR-363 with its clinicopathological characteristics was analyzed as well. The expression of RUNX3 in the experiment group was significantly lower than that in the control group (P<0.05). The expression level of miR-363 was significantly lower than in the control group (P<0.05). However, there was a correlation with tumor size, degree of differentiation, lymph node metastasis, depth of invasion and clinical stages (P<0.05). RUNX3 and miR-363 were significantly positively correlated with the degree of differentiation (r=0.7381, r=0.5375; P<0.05); RUNX3 and miR-363 were significantly negatively correlated with clinical stages (r=-0.7167, -0.6700; P<0.05). The area under the ROC curve of the combined test was larger than the single test. The expression of RUNX3 gene and miR-363 in peripheral blood of patients with colorectal cancer was lower than in the normal controls. The low expression of RUNX3 and miR-363 was closely related to various biological behaviors of colorectal cancer. A potential reference is provided for the evaluation of patients with colorectal cancer and expected to have an important guiding effect in the treatment of colorectal cancer. Moreover, combined test of RUNX3 and miR-363 has important significance in the diagnosis and treatment evaluation of colorectal cancer.
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Following the publication of the above article and a corrigendum in 2018 that corrected details of the correspondence information for authors, errors made in Fig. 5 and the funding details (doi: 10.3892/mmr.2018.9117), an interested reader drew to the authors’ attention that, in Fig. 6 on p. 8515 showing the results of cell migration and invasion assay experiments, a pair of data panels were overlapping, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original source. After having consulted their original data, the authors have realized that Fig. 6 was assembled incorrectly, The revised version of Fig. 6, now showing the correct data for the ‘ACHN/migratory/NC’ experiment, is shown on the next page. Note that all the authors approve of the publication of this corrigendum, and the authors are grateful to the Editor of Molecular Medicine Reports for granting them the opportunity to publish this. The authors regret their oversight in allowing this error to be included in the paper, and also apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 8510‑8517, 2018; DOI: 10.3892/mmr.2018.8899]
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Beclin 1 is involved in autophagy, differentiation, apoptosis and cancer progression, and functions as a haploinsufficient tumor suppressor gene. The aim of the present study was to elucidate the function of Beclin 1 in colon cancer. A Beclin 1-expressing plasmid was transfected into HCT-15 and HCT-116 cells, and the phenotypes and associated molecules were determined. Beclin 1 transfectants were subcutaneously injected into nude mice to determine tumor growth, and proliferation and apoptosis levels using Ki-67 immunostaining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), respectively. Beclin 1 overexpression inhibited viability as determined using a Cell Counting Kit-8 assay, inhibited migration and invasion as determined using a wound healing assay or Transwell assay, and lamellipodia formation by filamentous actin staining, induced autophagy as determined using electron microscopy, and light chain 3B (LC-3B) expression, and apoptosis as determined using Annexin V staining in the two cell lines (P<0.05). Beclin 1 induced G2 arrest of HCT-15 transfectants as determined using propidium iodide staining (P<0.05), whereas HCT-116 transfectants were arrested in G1 phase (P<0.05). The two transfectants exhibited increased expression of c-Myc, cyclin D1, β-catenin, insulin-response element 1 and 78 kDa glucose-regulated protein compared with the control and mock cells as determined using the reverse transcription-quantitative polymerase chain reaction (P<0.05). Beclin 1 overexpression upregulated LC-3B and cyclin-dependent kinase 4 expression, but downregulated cyclin E expression of the cancer cell lines as determined using western blot analysis (P<0.05). Beclin 1 expression in vivo significantly suppressed the proliferation of colon cancer cells in xenograft models via inducing apoptosis by TUNEL, and inhibiting proliferation by Ki-67 expression (P<0.05). Beclin 1 overexpression may reverse aggressive phenotypes and suppress colon cancer tumor growth, and be employed as a target molecule for gene therapy of patients with colon cancer.
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Epithelial-mesenchymal transition( EMT) is the phenomenon that epithelial cells transform to motile mesenchymal cells in the specific microenvironment. This phenomenon can be observed in invasion and metastasis of primary hepatocellular carcinoma. Therefore,this article will not only review EMT and it's regulatory factors,but also the role of EMT in the invasion and metastasis of primary liver cancer.
Liver Cancer
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The purpose of the present study was to investigate the serum levels of microRNA (miRNA/miR)-382-3p, -598-3p, -1246 and -184 in breast cancer patients and to assess their feasibility as biomarkers for breast cancer screening. Serum samples were obtained from 100 breast cancer patients and 40 age-matched healthy control subjects in Taizhou Central Hospital (Taizhou, Zhejiang, China) between January 2013 and September 2014. The serum expression levels of miR-382-3p, -598-3p, -1246 and -184 were determined by stem-loop reverse transcription-quantitative polymerase chain reaction. Receiver operating characteristic curves were drawn to evaluate the sensitivity and specificity of the serum miRNA expression levels for the screening of breast cancer. miR-382-3p and -1246 were significantly upregulated in the serum of the breast cancer patients, while miR-598-3p and -184 were significantly downregulated. The sensitivity and specificity to detect breast cancer were as follows: miR-382-3p, 52.0 and 92.5%; miR-598-3p, 95.0 and 85.0%; miR-1246, 93.0 and 75.0%; and miR-184, 87.5 and 71.0%, respectively. The expression levels of the four serum miRNAs were not correlated with the patients' clinical stage. In summary, miR-382-3p, -598-3p, -1246 and -184 are all involved in the development of breast cancer, and are promising biomarkers for breast cancer detection.
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