Transforming capacity of two novel genes JS-1 and JS-2 located in chromosome 5p and their overexpression in human esophageal squamous cell carcinoma

Fatima, Sarwat; Chui, Chung Hin; Tang, Wing Ka; Hui, Kin S; Au, Ho Wah; Li, Wing Y; Wong, Man Sau; Cheung, Filly; Tsao, Sai Wah; Lam, Alfred King‐Yin; Beh, SL; Wong, John; Law, Simon; Srivastava, Gopesh; Ho, Kin‐Yip; Chan, Albert S. C.; Tang, Johnny Cheuk On

doi:10.3892/ijmm.17.1.159

Cited by 11 publications

(31 citation statements)

References 41 publications

(45 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, deletion of JS‐2 was also common in both colorectal lesions and with almost half of each showing deletion. It is worth noting that previous work on JS‐2 has shown that deliberate overexpression of JS‐2 by transfection into NIH 3T3 cells caused no change to the ability of those cells to form colonies (Fatima et al., 2006). While JS‐2 may have some other role to play in tumour biology, it seems likely that the amplification or deletion of the gene seen in this study is coincidental to the generalised amplification/deletion of 5p in these cancers.…”

Section: Discussionmentioning

confidence: 95%

“…In our previous study on oesophageal squamous cell carcinoma, JS‐2 mRNA expression was studied in only 22 cases. Of these, 14% (3/22) and 9% (2/22) showed overexpression and decreased expression of JS‐2 mRNA respectively (Fatima et al., 2006). The majority of the cases showed no alterations of JS‐2 mRNA expression.…”

Section: Discussionmentioning

confidence: 99%

“…This implies that JS‐2 down regulation may have some role in the carcinogenesis or may be regulated in concert with other genes. The methodology of our previous study on the JS‐2 gene was attempting to determine its oncogenicity and would not have detected a possible function as a tumour suppressor (Fatima et al., 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Using semi‐quantitative real‐time polymerase chain reaction, overexpression of JS‐2 was noted in 18% (2/11) of oesophageal squamous cell carcinoma cell lines and in 14% (3/22) of tissues from patients with oesophageal squamous cell carcinoma (Fatima et al., 2006). Also, expression of JS‐2 was noted in 4% (1/22) of squamous dysplasia of oesophagus.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Altered JS‐2 expression in colorectal cancers and its clinical pathological relevance

Lam¹,

Gopalan²,

Nassiri³

et al. 2011

Molecular Oncology

View full text Add to dashboard Cite

Mucinous Adenocarcinoma Adenoma JS-2 gene A B S T R A C TJS-2 is a novel gene located at 5p15.2 and originally detected in primary oesophageal cancer.There is no study on the role of JS-2 in colorectal cancer. The aim of this study is to determine the gene copy number and expression of JS-2 in a large cohort of patients with colorectal tumours and correlate these to the clinicopathological features of the cancer patients. We evaluated the DNA copy number and mRNA expression of JS-2 in 176 colorectal tissues (116 adenocarcinomas, 30 adenomas and 30 non-neoplastic tissues) using real-time polymerase chain reaction. JS-2 expression was also evaluated in two colorectal cancer cell lines and a benign colorectal cell line. JS-2 amplification was noted in 35% of the colorectal adenocarcinomas. Significant differences in relative expression levels for JS-2 mRNA between different colorectal tissues were noted ( p ¼ 0.05). Distal colorectal adenocarcinoma had significantly higher copy number than proximal adenocarcinoma ( p ¼ 0.005). The relative expression level of JS-2 was different between colonic and rectal adenocarcinoma ( p ¼ 0.007).Mucinous adenocarcinoma showed higher JS-2 expression than non-mucinous adenocarcinoma ( p ¼ 0.02). Early T-stage cancers appear to have higher JS-2 copy number and lower expression of JS-2 mRNA than later stage cancers ( p ¼ 0.001 and 0.03 respectively). Colorectal cancer cell lines showed lower expression of JS-2 than the benign colorectal cell line. JS-2 copy number change and expression were shown for the first time to be altered in the carcinogenesis of colorectal cancer. In addition, genetic alteration of JS-2 was found to be related to location, pathological subtypes and staging of colorectal cancer.

show abstract

Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Altered JS‐2 expression in colorectal cancers and its clinical pathological relevance

Lam¹,

Gopalan²,

Nassiri³

et al. 2011

Molecular Oncology

View full text Add to dashboard Cite

show abstract

“…The formula used to calculate Td was: Td = (t1-t2) × lg2/lg(N t1 /N t2 ), where t1 and t2 are the time in h, N t1 is the cell number at t1, and N t2 is the cell number at time t2. 14 In vivo tumor model. The HCT116/siNS, HCT116/sihTERT and parental cell lines were expanded in vitro then injected hypodermically into six athymic nude mice (BALB/cA nu/nu, aged 4 to 5 weeks).…”

Section: Methodsmentioning

confidence: 99%

hTERT-targeted RNA interference inhibits tumorigenicity and motility of HCT116 cells

Shen¹,

Zhang²,

Zhang³

et al. 2008

Cancer Biology & Therapy

View full text Add to dashboard Cite

Telomerase is proposed as an anticancer target. Increasing evidence suggests that telomerase is involved in functions independent of telomere-extension activity. In this study, we designed a small interfering RNA (siRNA) targeting human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase. Using transient and persistent transfection of hTERT siRNA into telomerase-positive human colon carcinoma HCT116 cells, we demonstrated that hTERT siRNA suppresses hTERT expression and leads to inhibition of telomerase activity and HCT116 cell growth and in vivo tumorigenicity in nude mice. Further analysis indicated that depletion of hTERT reduces cell adhesion, migration, and invasion prior to inhibition of cell proliferation. Downregulation of hTERT also decreased the expression levels of adhesion-and motility-related proteins, in particular c-Met and integrins. The lack of detectable changes in telomere length showed that downregulation of hTERT in the present system had no significant effect on telomere-extension activity. Taken together, our results highlight the therapeutic potential of a novel hTERT siRNA and suggest that hTERT is involved in the regulation of cell motility in a telomere-independent manner.

show abstract

Cellular and Molecular Biology of Esophageal Cancer

Lam

2019

Esophageal Cancer

View full text Add to dashboard Cite

The study of cellular and molecular biology in esophageal carcinomas could serve the following purposes: (1) to establish the presence or absence of an infectious co-factor such as human papilloma virus; (2) to understand the genetic mechanisms of disease such as genetic mutations, changes in microRNAs changes as well as the roles of cancer stem cells; (3) to provide prognostic information; and (4) to predict response to medical therapies and new modalities of treatment. In recent years, major genomic information obtained from the whole genomic sequencing of prospectively collected frozen samples of esophageal carcinomas open the field for in-depth understanding of the complex molecular pathway of the cancer. The Anti-Her 2 therapy was approved internationally as targeted therapy for esophageal adenocarcinoma at the gastroesophageal junction. Assessment of Her 2 expression is the most important molecular test to be performed properly in clinical settings. The study of cellular and molecular biology in esophageal carcinomas depends on the properly collected formalin fixed as well as snap frozen tissues and blood from the patients. Tissue microarray and whole-slide scanning technologies allow tissue research in esophageal carcinomas to be progressed in a more efficient way. Cancer cell lines and animal models could use to study the functional aspects of the various cellular and molecular changes in esophageal carcinomas.

show abstract

Transforming capacity of two novel genes JS-1 and JS-2 located in chromosome 5p and their overexpression in human esophageal squamous cell carcinoma

Cited by 11 publications

References 41 publications

Altered JS‐2 expression in colorectal cancers and its clinical pathological relevance

Altered JS‐2 expression in colorectal cancers and its clinical pathological relevance

hTERT-targeted RNA interference inhibits tumorigenicity and motility of HCT116 cells

Cellular and Molecular Biology of Esophageal Cancer

Contact Info

Product

Resources

About