Loss of p15<sup>INK4b</sup>Expression in Colorectal Cancer is Linked to Ethnic Origin

Abdel‐Rahman, Wael M.; Nieminen, Taina T.; Shoman, Soheir; Eissa, Saad; Peltomäki, Païvi

doi:10.7314/apjcp.2014.15.5.2083

Cited by 3 publications

(4 citation statements)

References 30 publications

(22 reference statements)

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“…Despite curative therapy, most patients still experience disease relapse within 5 years which lead to morbidity and ultimately mortality (Wilkinson and Scott-Conner 2008;Wolpin and Mayer 2008). Clinical trials for CRC have focused mainly on prevention and early detection of the disease and selection of suitable patients for adjuvant therapy (Walsh and Terdiman 2003;Boursi and Arber 2007;Andre et al, 2009;Lee et al, 2013;Abdel-Rahman et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Lack of Prognostic Significance of SOCS-1 Expression in Colorectal Adenocarcinomas

Ayyildiz¹,

Dolar²,

Adım³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Introduction: Recent studies have indicated that down-regulation of the suppressor of cytokine signaling-1 (SOCS-1) gene results in tumor formation and that SOCS-1 acts as a tumor suppressor gene. SOCS-1 has been also suggested to function as a tumor suppressor with colorectal cancer. Objectives: In the present study, we aimed to determine the association of SOCS-1 expression in colorectal cancer tissues with clinicopathologic characteristics immunohistochemically and also to identify its prognostic significance. Materials and Methods: SOCS-1 expression was studied immunohistochemically in 67 patients diagnosed with resected colorectal carcinomas and 30 control subjects. Results: SOCS-1 expression was found in 46.3% of tumor tissues and 46.7% of the control group. Statistical analyses did not establish any significant association between SOCS-1 expression and clinicopathologic characteristics. Also, no significant association with SOCS-1 expression was found using progression-free survival and overall survival analyses (p=0.326 and p=0.360, respectively). Conclusions: Our results show that SOCS-1 has no prognostic significance in colorectal cancer.

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Section: Introductionmentioning

confidence: 99%

Lack of Prognostic Significance of SOCS-1 Expression in Colorectal Adenocarcinomas

Ayyildiz¹,

Dolar²,

Adım³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Immunohistochemical analyses for detection of CNN3 in uncultured colorectal cancer specimens were performed on 57 FFPE tissue sections derived from a series described in previous publications[21,22]. CNN3 expression was detected as cytoplasmic expression in smooth muscle and endothelial cells, stromal fibroblasts, and germinal centers of lymphoid follicles.…”

Section: Resultsmentioning

confidence: 99%

“…Additional features of this series are included in Table 1. Molecular characterization of these tumors was described in our previous work[21,22]. We used the Envision+DAB system and immunohistochemistry staining protocol as previously described[23].…”

Section: Methodsmentioning

confidence: 99%

“…Extracellular mucin was detected morphologically after staining with hematoxylin and eosin as well as Periodic Acid-Schiff. Microsatellite instability was detected by the microsatellite markers BAT25 and BAT26; p53 status was characterized by immunohistochemical detection of protein stabilization[21,22]. NS: Not significant; MSI: Microsatellite instability; MSS: Microsatellite stable; CNN3: Calponin 3.…”

Section: Methodsmentioning

confidence: 99%

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Calponin 3 promotes invasion and drug resistance of colon cancer cells

Nair¹,

Alkhayyal²,

Sivaramakrishnan³

et al. 2019

WJGO

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BACKGROUNDCalponin 3 (CNN3) is an actin-binding protein expressed in smooth muscle and non-smooth muscle cells. It is required for cytoskeletal rearrangement and wound healing.AIMTo dissect the role of CNN3 in carcinogenesis with a focus on colon cancer.METHODSA total of 20 cancer cell lines (8 breast, 11 colon, and HeLa cervical cancer cell as a positive control for mesenchymal phenotype) and 57 formalin-fixed, paraffin-embedded sections from archived sporadic colorectal carcinomas were included in this study. CNN3 expression analysis by western blot or immunohistochemistry was followed by functional analyses. The CNN3 gene was silenced by specific small interfering RNA (commonly known as siRNA), followed by confirmation of the silencing efficiency by western blotting. Then, the silenced cells and control siRNA-transfected cells were analyzed for changes in epithelial and mesenchymal markers, invasion, and response to 5-fluoruracil treatment. We also performed proteomics analysis using a phospho-kinase array-based panel of 45 proteins.RESULTSCNN3 showed positive expression in 6/8 breast and 9/11 colon cancer lines and in HeLa cells. Interestingly, the colorectal adenocarcinoma line SW480 was negative, while the cell line developed from its matching lymph node metastasis (SW620) was positive for CNN3. CNN3 expression was fairly consistent with the metastatic phenotype in colon cancer because it was absent in one other colon cell line from a primary site and expressed in all others. We selected SW620 for subsequent functional analyses. CNN3-silenced SW620 cells showed a reduction in collagen invasion and loss of mesenchymal markers. CNN3 silencing caused an increase in the SW620 colon cancer cell sensitivity to 5-fluorouracil. Phospho-kinase array-based proteomics analysis showed that CNN3 silencing in SW620 reduced extracellular signal-regulated kinase, β-Catenin, mutant p53, c-Jun, and heat shock protein 60 activities but increased that of checkpoint kinase 2. CNN3 was expressed in 20/57 (35%) colon cancer cases as shown by immunohistochemistry. CNN3 was associated with a decrease in overall survival in colon cancer in silico.CONCLUSIONThese results show the involvement of CNN3 in lymph node metastasis and resistance to chemotherapy in colon cancer and suggest that significant oncogenic pathways are involved in these CNN3-related actions.

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The Role of Stem Cell DNA Methylation in Colorectal Carcinogenesis

Song

2016

Stem Cell Rev and Rep

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Stems cells of the colon crypt are the origin of colon mature cells. Colorectal cancer cells are also suggested to originate from crypt stem cells undergoing a series of epigenetic and genetic alterations. Aberrant methylation plays important roles in early carcinogenesis and lead to altered gene expression and regulation, resulting in accumulation of damages to cell function and ultimately, malignant transformation. Aberrances in hypermethylation and hypomethylation act in different mechanism through the regulation of various genes during CSC carcinogenesis, and both of them play crucial roles in stem cell differentiation towards cancer cells. A large majority of epigenetic and genetic abnormalities that work coordinately in colorectal carcinogenesis are related to cell growth and division, indicating that the intrinsic abnormalities of CRC lie in dysregulation of basic cellular processes. Detection of abnormal methylation can be used in cancer screening and early detection, while reversal of aberrant methylation using drugs may have potential in cancer therapy. This review will provide an overview on the roles of aberrant methylation and a summary of genes that are affected during CRC carcinogenesis.

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Loss of p15^INK4bExpression in Colorectal Cancer is Linked to Ethnic Origin

Cited by 3 publications

References 30 publications

Lack of Prognostic Significance of SOCS-1 Expression in Colorectal Adenocarcinomas

Lack of Prognostic Significance of SOCS-1 Expression in Colorectal Adenocarcinomas

Calponin 3 promotes invasion and drug resistance of colon cancer cells

The Role of Stem Cell DNA Methylation in Colorectal Carcinogenesis

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Loss of p15INK4bExpression in Colorectal Cancer is Linked to Ethnic Origin

Cited by 3 publications

References 30 publications

Lack of Prognostic Significance of SOCS-1 Expression in Colorectal Adenocarcinomas

Lack of Prognostic Significance of SOCS-1 Expression in Colorectal Adenocarcinomas

Calponin 3 promotes invasion and drug resistance of colon cancer cells

The Role of Stem Cell DNA Methylation in Colorectal Carcinogenesis

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Loss of p15^INK4bExpression in Colorectal Cancer is Linked to Ethnic Origin