Colon cancer

Labianca, Roberto; Beretta, Giordano Domenico; Gatta, Gemma; Braud, Filippo de; Wils, J.

doi:10.1016/j.critrevonc.2004.03.003

Cited by 37 publications

(21 citation statements)

References 176 publications

(182 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Despite progress in early diagnosis and treatment of this cancer, aggressive surgical or chemotherapeutic interventions have not significantly improved the prognosis of patients with the advanced disease, particularly peritoneal carcinomatosis. 12 Recently, reports showed that the abnormal expression of RCK/p54 was closely related to malignant transformation and progression of colorectal cancer. 5 The RCK protein, RCK/p54, which is a 54-kDa cytoplasmic protein belonging to the DEAD …”

Section: Discussionmentioning

confidence: 99%

Knockdown of RCK/p54 expression by RNAi inhibits proliferation of human colorectal cancer cells in vitro and in vivo

Lin¹,

Wang²,

Shen³

et al. 2008

Cancer Biology & Therapy

View full text Add to dashboard Cite

Colorectal cancer is the third most common cancer in both men and women around the world. Although much progress of the mechanism of colorectal carcinogenesis has been made, the studies centering on the mechanisms of tumorigenesis are much needed to be further exploited. The overexpression of RCK/p54 gene, a member of the DEAD box protein/RNA helicase family, has been found in this malignancy. Roles of RCK in the development of colon cancer, however, are unknown. In this report, we explored whether RCK/p54 plays a role in maintaining the malignant phenotype and functions in the canonical Wnt signaling pathway of colorectal cancer cells harboring an APC mutation. The ectopic overexpression of RCK/p54 gene in colorectal cancer cells by transfection with RCK/p54 cDNA could lead to a significant increase of Tcf transcriptional activity and expression levels of Wnt target genes. By RNAi assay, we also observed that the Tcf transcriptional activity in LoVo-shRNA cells was significantly decreased by approximately 61.3%, while the mRNA and protein expression levels of Wnt target genes were also obviously decreased. Furthermore, the anti-tumour effects and its possible mechanisms of actions in LoVo cells elicited by a decrease in the level of RCK/ p54 by RNAi were examined. Results showed that RCK/p54 downregulation could significantly reduce the viability of LoVo cells, increased cell number of S phase, led to cell apoptosis induction, and inhibited tumor growth in nude mice. Taken together, RCK/ p54 might be a determinant of colorectal cancer proliferation by activating the canonical Wnt pathway and RCK/p54-shRNA might be a potential strategy for colorectal cancer gene therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Knockdown of RCK/p54 expression by RNAi inhibits proliferation of human colorectal cancer cells in vitro and in vivo

Lin¹,

Wang²,

Shen³

et al. 2008

Cancer Biology & Therapy

View full text Add to dashboard Cite

show abstract

“…There is a growing body of evidence that an individual's susceptibility to sCRC depends on both his/her an individual's genetic profile (so called "genetic makeup") and exposure to exogenous and endogenous carcinogens (DNA damaging agents) [3,4].…”

Section: Introductionmentioning

confidence: 99%

The C/A polymorphism in intron 11 of the XPC gene plays a crucial role in the modulation of an individual’s susceptibility to sporadic colorectal cancer

et al. 2011

View full text Add to dashboard Cite

Abstract:Background: Epidemiological data show that colorectal cancer (CRC) is the second most frequent malignancy worldwide. The involvement of "minor impact genes" such as XME and DNA-repair genes in the etiology of sporadic cancer has been postulated by other authors.Aim: we focused on analyzing polymorphisms in DNA-repair genes in CRC. We considered the following genes involved in DNA-repair pathways: base excision repair (OGG1 Ser326Cys, XRCC1 Trp194Arg and Arg399Gln); nucleotide excision repair [XPA (-4)G/A, XPC C/A (i11) and A33512C (Lys939Gln), XPD Asp312Asn and A18911CMaterial and methods: The study group consisted of 133 patients diagnosed with sporadic CRC, while the control group was composed of 100 age-matched non-cancer volunteers. Genotyping was performed by PCR and PCR-RFLP. Fisher's exact test with a Bonferroni correction for multiple testing was used.Results: We found that: i) XPC C/A (i11) heterozygous variant is associated with increased risk of CRC [OR is 2.07 (95% CI 1.1391,3.7782) p=0.038], ii) XPD A18911C (Lys751Gln) is associated with decreased risk of CRC [OR=0.4497, (95% CI 0.2215,0,9131) p=0.031] for an individual with at least one A allele at this locus. Conclusions:1. the XPC C/A (i11) genotype is associated with an increased risk of sporadic colorectal cancer.2. the NER pathway has been highlighted in our study, as a most important in modulation of individual susceptibility to sCRC.

show abstract

“…The incidence is high, especially in developed countries, and it is now rising in developing countries like Thailand (Labianca et al, 2004;Khuhaprema and Srivatanakul, 2008). Genetics, environment, lifestyle, and diet are considered important factors that contribute to the development of colon cancer.…”

Section: Introductionmentioning

confidence: 99%

Effects of silk sericin on the proliferation and apoptosis of colon cancer cells

et al. 2012

View full text Add to dashboard Cite

Sericin is a silk protein woven from silkworm cocoons (Bombyx mori). In animal model, sericin has been reported to have anti-tumoral action against colon cancer. The mechanisms underlying the activity of sericin against cancer cells are not fully understood. The present study investigated the effects of sericin on human colorectal cancer SW480 cells compared to normal colonic mucosal FHC cells. Since the size of the sericin protein may be important for its activity, two ranges of molecular weight were tested. Sericin was found to decrease SW480 and FHC cell viability. The small sericin had higher anti-proliferative effects than that of the large sericin in both cell types. Increased apoptosis of SW480 cells is associated with increased caspase-3 activity and decreased Bcl-2 expression. The anti-proliferative effect of sericin was accompanied by cell cycle arrest at the S phase. Thus, sericin reduced SW480 cell viability by inducing cell apoptosis via caspase-3 activation and down-regulation of Bcl-2 expression. The present study provides scientifi c data that support the protective effect of silk sericin against cancer cells of the colon and suggests that this protein may have signifi cant health benefi ts and could potentially be developed as a dietary supplement for colon cancer prevention.

show abstract

Colon cancer

Cited by 37 publications

References 176 publications

Knockdown of RCK/p54 expression by RNAi inhibits proliferation of human colorectal cancer cells in vitro and in vivo

Knockdown of RCK/p54 expression by RNAi inhibits proliferation of human colorectal cancer cells in vitro and in vivo

The C/A polymorphism in intron 11 of the XPC gene plays a crucial role in the modulation of an individual’s susceptibility to sporadic colorectal cancer

Effects of silk sericin on the proliferation and apoptosis of colon cancer cells

Contact Info

Product

Resources

About