K-ras 4A and 4B are co-expressed widely in human tissues, and their ratio is altered in sporadic colorectal cancer

Journal of Experimental and Clinical Cancer Research

Volumn 25, Issue 2, 2006, Pages 259-267

  Plowman, S J ^a   Berry, R L ^a   Bader, S A ^a   Luo, F ^b   Arends, M J ^b   Harrison, D J ^a   Hooper, M L ^a   Patek, Charles E ^a  

^a UNIVERSITY OF EDINBURGH   (United Kingdom)

^b UNIVERSITY OF CAMBRIDGE   (United Kingdom)

Author keywords

Alternative splicing; Colorectal cancer; K ras

Indexed keywords

GELATINASE A; K RAS PROTEIN; PROTEIN K RAS 4A; PROTEIN K RAS 4B; UNCLASSIFIED DRUG;

ARTICLE; CANCER CELL CULTURE; CANCER INVASION; CELL MIGRATION; CHROMOSOME VARIANT; COLON ADENOCARCINOMA; COLON CARCINOGENESIS; COLON CARCINOMA; COLORECTAL CANCER; CONTROLLED STUDY; GENE EXPRESSION; GENE MUTATION; HUMAN; HUMAN CELL; HUMAN TISSUE; LUNG CANCER; METASTASIS; ONCOGENE K RAS; PANCREAS CANCER; PRIORITY JOURNAL; PROTEIN EXPRESSION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION;

ADENOCARCINOMA; COLON; COLORECTAL NEOPLASMS; DNA MUTATIONAL ANALYSIS; GENES, RAS; HUMANS; MUTATION; PROTEIN ISOFORMS; RNA, MESSENGER; TUMOR CELLS, CULTURED;

EID: 33746381948     PISSN: 03929078     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (45)

1. Toms J.R.: In: CancerStats Monograph 2004. London: Cancer Research UK, 2004.
2. Grady W.M., Markowitz S.D.: Genetic and epigenetic alterations in colon cancer. Ann. Rev. Genomics. Hum. Genet. 3: 101-128, 2002.
3. Kalnina Z., Zayakin P., Silina K., Line A.: Alterations of pre-mRNA splicing in cancer. Genes Chromosomes Cancer 42: 342-357, 2005.
4. Venables J.P.: Aberrant and alternative splicing in cancer. Cancer Res. 64: 7647-7654, 2004.
5. Capon D.J., Seeburg, P.H., McGrath J.P., et al.: Activation of Ki-ras2 gene in human colon and lung carcinomas by two different point mutations. Nature 304: 507-513, 1983.
6. Ehrhardt A., Ehrhardt G.R.A., Guo, X., Schrader J.W.: Ras and relatives - job sharing and networking keep an old family together. Exp. Hematol. 30: 1089-1106, 2002.
7. Cox A.D., Der C.J.: The dark side of Ras: regulation of apoptosis. Oncogene 22: 8999-9006, 2003.
8. Conlin A., Smith G., Carey F.A., Wolf C.R., Steele R.J.: The prognostic significance of K-ras, p53 and APC mutations in colorectal carcinoma. Gut 54: 1283-1286, 2005.
9. Cheng L., Lai M-F.: Aberrant crypt foci as microscopic precursors of colorectal cancer. World J. Gastroenterology 9: 2642-2649, 2003.
10. Yamada S., Yashiro M., Maeda K., Nishiguchi Y., Hirakawa K.: A novel high-specificity approach for colorectal neoplasia: Detection of K-ras2 oncogene mutation in normal mucosa. Int. J. Cancer 113: 1015-1021, 2005.
11. Fisher G.H., Wellen S.L., Klimstra D., et al.: Induction and apoptotic regression of lung adenocarcinomas by regulation of a K-Ras transgene in the presence and absence of tumour suppressor genes. Genes. Develop. 15: 3249-3262, 2001.
12. Nakano M., Aoki K., Matsumoto N., et al.: Suppression of colorectal cancer growth using an adenovirus vector expressing an antisense K-ras RNA. Mol. Therapy. 3: 491-499, 2001.
13. Janssen K.P., Marjou F., Pinto D., et al.: Targeted expression of oncogenic K-ras in intestinal epithelium causes spontaneous tumourigenesis in mice. Gastroenterology 123: 492-504, 2002.
14. Pells S., Divjak M., Romanowski P., et al.: Developmentally-regulated expression of murine K-ras isoforms. Oncogene 15: 1781-1786, 1997.
15. Butz J.A., Roberts K.G., Edwards J.S.: Detecting changes in the relative expression of KRAS2 splice variants using polymerase colonies. Biotechnol. Prog. 20: 1836-1839, 2004.
16. Voice J.K., Klemke R.L., Le A., Jackson J.H.: Four human ras homologs differ in their abilities to activate Raf-1, induce transformation, and stimulate cell motility. J. Biol. Chem. 274: 17164-17170, 1999.
17. Zhang Z., Wang Y., Vikis H.G., et al.: Wildtype Kras2 can inhibit lung carcinogenesis in mice. Nature Genet. 29: 25-33, 2001.
18. James R.M., Arends M.J., Plowman S.J., et al.: K-ras protooncogene exhibits tumour suppressor activity as its absence promotes tumourigenesis in murine teratomas. Mol. Cancer Res. 1: 820-825, 2003.
19. Potenza N., Vecchione C., Notte A., et al.: Replacement of K-Ras with K-Ras supports normal embryonic development despite inducing cardiovascular pathology in adult mice. EMBO. Reports 6: 432-437, 2005.
20. Liao J., Wolfman J.C., Wolfman A.: K-Ras regulates the steady-state expression of matrix metalloproteinase 2 in fibroblasts. J. Biol. Chem. 278: 31871-31878, 2003.
21. Plowman S.J., Arends M.J., Brownstein D.G., et al.: The K-Ras 4A isoform promotes apoptosis but does not affect either lifespan or spontaneous tumor incidence in aging mice. Exp. Cell Res. 312: 16-26, 2006.
22. Wang Y., You M., Wang Y: Alternative splicing of the K-ras gene in mouse tissues and cell lines. Exp. Lung Res. 27: 255-267, 2001.
23. Plowman S.J., Williamson D.J., O'Sullivan M.J., et al.: While K-ras is essential for mouse development, expression of the K-ras 4A splice variant is dispensable. Mol. Cell. Biol. 23: 9245-9250, 2003.
24. Johnson L., Greenbaum D., Cichowski K., et al.: K-ras is an essential gene in the mouse with partial functional overlap with N-ras. Genes Dev. 11: 2468-2481, 1997.
25. Morris R.G., Curtis L.J., Romanowski P., et al.: Ki-ras mutations in adenomas: a characteristic of cancer-bearing colorectal mucosa. J. Path. 180: 357-363, 1996.
26. Gayet J., Zhou X. P., Duval A., et al.: Extensive characterisation of genetic alterations in a series of human colorectal cancer cell lines. Oncogene 20: 5025-5032, 2001.
27. Zhu D., Keohavong P., Finkelstein S.D., et al.: K-ras mutations in normal colorectal tissues from K-ras mutation-positive colorectal cancer patients. Cancer Res 57: 2485-2492, 1997.
28. McGrath J.P., Capon D.J., Smith D.H., et al.: Structure and organisation of the human Ki-ras proto-oncogene and a related processed pseudogene. Nature 304: 501-506, 1983.
29. Losi L., Baisse B., Bouzourene H., Benhattar J.: Evolution of intratumoral heterogeneity during colorectal cancer progression. Carcinogenesis 26: 916-922, 2005.
30. Ghigna C., Moroni M., Porta C., Riva S., Biamonti G.: Altered expression of heterogeneous nuclear ribonucleoproteins and SR factors in human colon adenocarcinomas. Cancer Res. 58: 5818-5824, 1998.
31. Li J., Mizukami Y, Zhang X., Jo W-S., Chung D.C.: Oncogenic K-ras stimulates Wnt signaling in colon cancer through inhibition of GSK-3b. Gastroenterology 128: 1907-1918, 2005.
32. Pollock C.B., Shirasawa S., Sasasuki T., Kolch W., Dhillon A.S.: Oncogenic K-RAS is required to maintain changes in cytoskeletal organization, adhesion, and motility in colon cancer cells. Cancer Res. 65: 1244-1250, 2005.
33. Smakman N., Borel Rinkes I.H., Voest E.E., Kranenburg O.: Control of colorectal metastasis formation by K-Ras. Biochim. Biophys. Acta 1756: 103-114, 2005.
34. Papadopoulou S., Scorilas A., Arnogianaki N., et al.: Expression of Gelatinase-A (MMP-2) in human colon cancer and normal colon mucosa. Tumor Biol. 22: 383-389, 2001.
35. Ornstein D.L., Cohn K.H.: Balance between activation and inhibition of matrix metalloproteinase-2 (MMP-2) is altered in colorectal tumours compared to normal colonic epithelium. Digestive Diseases Sci. 47: 1281-1830, 2002.
36. Yoon W-H., Jung Y-J., Kim T-D., et al.: Gabexate mesilate inhibits colon cancer growth, invasion, and metastasis by reducing matrix metalloproteinases and angiogenesis. Clin. Cancer Res. 10: 4517-4526, 2004.
37. Li B.H., Zhao P., Liu S.Z., Yu Y.M., Han M., Wen J.K.: Matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 in colorectal carcinoma invasion and metastasis. World J. Gastroenterol. 11: 3046-3050, 2005.
38. Hesson L.B., Wilson R., Morton D., et al.: CpG island promoter hypermethylation of a novel Ras-effector gene RASSF2A is an early event in colon carcinogenesis and correlates inversely with K-ras mutations. Oncogene 24: 3987-3994, 2005.
39. Al-Hajj M., Becker M.W., Wicha M., Weissman I., Clarke M.F: Therapeutic implications of cancer stem cells. Curr. Opin. Genet. Dev. 14: 43-47, 2004.
40. Diaz R.D., Ahn D., Lopez-Barcons L., et al.: The N-ras proto-oncogene can suppress the malignant phenotype in the presence or absence of its oncogene. Cancer Res. 62: 4514-4518, 2002.
41. Burdon T., Smith A., Savatier P.: Signalling, cell cycle and pluripotency in embryonic stem cells. Trends Cell. Biol. 12: 432-438, 2002.
42. Jang J-H., Shin K-H., Park Y-J., Lee R.J., McKeehan W.L., Park J.G.: Novel transcripts of fibroblast growth factor receptor 3 reveal aberrant splicing and activation of cryptic splice sequences in colorectal cancer. Cancer Res. 60: 4049-4052, 2000.
43. Huerta S., Srivatsan E.S., Venkatesan N., et al.: Alternative mRNA splicing in colon cancer causes loss of expression of neural cell adhesion molecule. Surgery 130: 834-843, 2001.
44. Patten L.C., Narasimhaswamy S., Belaguli D.V.M., et al.: Serum response factor is alternatively spliced in human colon cancer. J. Surgical Res. 121: 92-100, 2004.
45. Kole R., Williams T., Cohen L.: RNA modulation, repair and remodelling by splice switching oligonucleotides. Acta Biochemica Polonica 51: 373-378, 2004.