Gene expression profiling: Canonical molecular changes and clinicopathological features in sporadic colorectal cancers

Kim, Jin Cheon; Kim, Seon‐Young; Roh, Seon Ae; Cho, Dong‐Hyung; Kim, Dae Dong; Kim, Jeong Hyun; Kim, Yong‐Sung

doi:10.3748/wjg.14.6662

Cited by 26 publications

(19 citation statements)

References 47 publications

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“…However, the clinicopathological characteristics of SPRR3 have not been investigated in other types of cancers, including colorectal cancer. We have previously reported the association of several genes with molecular alterations in colorectal tumorigenesis (8). Surprisingly, in contrast to the findings in ESCC, SPRR3 was frequently and dramatically upregulated in colorectal cancers.…”

Section: Discussioncontrasting

confidence: 48%

“…To investigate the molecular changes associated with colorectal tumorigenesis, we analyzed gene expression patterns in 84 patients with sporadic colorectal cancer by using a microarray (8). Among 1263 differentially expressed genes, SPRR3 was shown to be associated with molecular changes, and we therefore examined the expression level of SPRR3 in colorectal cancers.…”

Section: Sprr3 Is Upregulated In Colorectal Cancermentioning

confidence: 99%

“…We previously identified several genes associated with molecular changes in sporadic colorectal cancers by microarray analysis of the gene expression profiles of sporadic colorectal cancer patients. When we investigated these genes, we found that SPRR3 (small proline rich repeat protein 3) was a protein associated with the molecular changes and clinicopathological features of this disease (8). SPRR proteins are known to be markers for terminal squamous cell differentiation, but they also function in nonsquamous tissues (9).…”

Section: Introductionmentioning

confidence: 99%

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Upregulation of SPRR3 Promotes Colorectal Tumorigenesis

Cho

Roh

et al. 2010

Mol Med

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Hereditary colorectal cancer develops through a series of well-defined genetic and histological changes. However, elucidation of the canonical pathway based on hereditary colorectal cancer has not provided a clear explanation of the molecular mechanisms of sporadic colorectal cancer. To identify the alterative pathways involved in sporadic colorectal tumorigenesis, we performed gene expression analysis in patients with sporadic colorectal tumors. A comparison analysis of gene expression profiles revealed a pattern of upregulation of small proline rich repeat protein 3 (SPRR3) in tumor samples. SPRR3 has previously been reported to be downregulated in esophageal cancer. However, in the present study, we observed that SPRR3 was strongly upregulated in 31 of 35 samples of sporadic colorectal tumors (88%). We also determined that overexpression of SPRR3 not only accelerates colorectal cancer cell proliferation but also is associated with lymphovascular invasion in colorectal cancer. Moreover, AKT was activated and p53 levels were decreased in cells that overexpressed SPRR3. In contrast to the pattern seen in esophageal cancer, these results suggest that increased expression of SPRR3 is involved in colorectal tumorigenesis.

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Section: Discussioncontrasting

confidence: 48%

Section: Sprr3 Is Upregulated In Colorectal Cancermentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Upregulation of SPRR3 Promotes Colorectal Tumorigenesis

Cho

Roh

et al. 2010

Mol Med

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“…LDHA expression is representative for increased pyruvate metabolism, which is associated with enhanced glycolysis. In line with the observed increase in expression of glycolysis and associated pathways is an apparent increase in LDHA expression in adenomas, while no change is observed during malignant transformation [17,18]. Hypoxia is one of the mechanisms that regulate transcriptional changes to support these metabolic alterations [19].…”

Section: Processes Reprogrammed During Adenoma Development and Genomimentioning

confidence: 52%

The adenoma hunt in colorectal cancer screening: defining the target

Sillars-Hardebol

Carvalho

Engeland

et al. 2011

The Journal of Pathology

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Colorectal adenomas are precursor lesions of colorectal cancer. Different biological and metabolic processes contribute to adenomagenesis. Subsequent progression to carcinoma occurs in only about 5% of the cases. Detection and removal of all adenomas would reduce CRC incidence and mortality, but at the cost of major over-treatment. Classical morphological characteristics fail to accurately discriminate between adenomas that will become malignant and those that will not. Understanding the biology of cancer development will help to better characterize adenomas at high risk of progression, and subsequently establish triage tests that allow to safely reserve colonoscopy only for individuals at high probability of having truly high-risk colorectal adenomas. Screening tests based on genomic changes that affect relevant biological and metabolic processes hold most promise in this respect.

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“…Thence, TRAPPC9 may adjust the function of trans-Golgi and the formation of autophagosome during cancer development. Studies have confirmed that transcription of TRAPPC9 exists in various cell lines and tumor tissues, and clinical studies have also reported TRAPPC9 transcripts with human breast [20] , colon cancer [21] , osteosarcoma [22] , and lymphoma [23,24] . Recent some genetic susceptibility studies of lung cancer have focus on single nucleotide polymorphisms (SNPs) in lncRNAs.…”

Section: Introductionmentioning

confidence: 81%