Role of hSRBC, a putative TSG, in development of primary cancer: a review

Paper Details

Review Paper 03/06/2024
Views (202) Download (25)
current_issue_feature_image
publication_file

Role of hSRBC, a putative TSG, in development of primary cancer: a review

Dipanjana Mazumder
Int. J. Biosci.24( 6), 13-17, June 2024.
Certificate: IJB 2024 [Generate Certificate]

Abstract

Multistep progression into cancer involves inactivation of tumor suppressor genes (TSGs) by deletion, methylation and mutation. Chr 11p15 has been found to be deleted in primary carcinoma of many tissues, including breast, cervix, stomach, lung, bladder cancer, etc. hSRBC, a candidate TSG located in chr 15.4, and associated with many molecular pathways, like PKC-δ, p53 and caveolin pathway may well be responsible for tumirogenesis.  hSRBC can induce cell cycle arrest and increase the apoptotic sensitivity of cells in stressed condition by stabilizing p53. hSRBC can also associate with caveolin when caveolae bud to form vesicles. hSRBC also effects localization of EGFR to caveolae through phosphorylation by PKC-δ. Thus, inactivation of hSRBC plays havoc inside the cell. Future hope may lie in restoring the function of hSRBC in cells and guiding the affected cells to apoptotic pathway instead of using radiation or chemotherapy.

VIEWS 67

Chunder N, Mandal S, Roy A, Roychoudhury S, Panda CK. 2004. Analysis of different deleted regions in chromosome 11 and their interrelations in early- and late-onset breast tumors: association with cyclin D1 amplification and survival. Diagnostic Molecular Pathology 13, 172-182. https://doi.org/10.1097/01.pas.0000124337.49401.0b

Gschwendt M. 1999. Protein kinase Cδ. European Journal of Biochemistry 259, 555–564.

Gustincich S, Schneider C. 1993.  Serum deprivation response gene is induced by serum starvation but not by contact inhibition. Cell Growth & Differentiation 4, 753-760.

Kozlowski L, Filipowski T, Rucinska M, Pepinski W, Janica J, Skawronska M, Poznanski J, Wojtukiewicz MZ. 2006. Loss of heterozygosity on chromosomes 2p, 3p, 18q21.3 and 11p15.5 as a poor prognostic factor in stage II and III (FIGO) cervical cancer treated by radiotherapy. Neoplasma 53, 440–443.

Lee JH, Byun DS, Lee MG, Ryu BK, Kang MJ, Chae KS, Lee KY, Kim HJ, Park H, Chi SG. 2008. Frequent epigenetic inactivation of hSRBC in gastric cancer and its implication in attenuated p53 response to stresses. International Journal of Cancer 122, 1573–1584. https://doi.org/10.1002/ijc.23166.

McMahon KN, Zajicek H, Li WP, Peyton MJ, Minna JD, Hernandez VJ, LubyPhelps K, Anderson RGW. 2009. SRBC/cavin-3 is a caveolin adapter protein that regulates caveolae function. The EMBO Journal 28, 1001–1015. https://doi.org/10.1038/emboj.2009.46.

Mineo C, Gill GN, Anderson RGW. 1999. Regulated migration of epidermal growth factor receptor from caveolae. The Journal of Biological Chemistry 274, 30636–30643.

Moskaluk CA, Rumpel CA. 1998. Allelic deletion in 11p15 is a common occurrence in esophageal and gastric adenocarcinoma. Cancer 83, 232–239.

Panani AD, Ferti AD, Raptis SA, Roussos C. 2004. Novel recurrent structural chromosomal aberrations in primary bladder cancer. Anticancer Research 24, 2967–2974.

Perletti G, Marras E, Dondi D, Osti D, Congiu T, Ferrarese R, de Eguileor M, Tashjian AH, Jr. 2005. p21Waf1/Cip1 and p53 are downstream effectors of protein kinase C delta in tumor suppression and differentiation in human colon cancer cells. International Journal of Cancer 113, 42–53. https://doi.org/10.1002/ijc.20535

Pulido HA, Fakruddin MJ, Chatterjee A, Esplin ED, Beleño N, Martinez G, Posso H, Evans GA, Murty VV. 2000. Identification of a 6-cM minimal deletion at 11q23.1-23.2 and exclusion of PPP2R1B gene as a deletion target in cervical cancer. Cancer Research 60, 6677-6682.

Rodriguez E, Rao PH, Ladanyi M, Altorki N, Albino AP, Kelsen DP, Jhanwar SC, Chaganti RS. 1990. 11p13-15 is a specific region of chromosomal rearrangement in gastric and esophageal adenocarcinomas. Cancer Research 50, 6410–6416.

Roy D, Calaf G, Hei TK. 2003. Allelic imbalance at 11p15.5-15.4 correlated with c-Ha-ras mutation during radiation-induced neoplastic transformation of human breast epithelial cells. International Journal of Cancer 103, 730–737. https://doi.org/10.1002/ijc.10895.

Smart EJ, Ying YS, Mineo C, Anderson RG. 1995. A detergent-free method for purifying caveolae membrane from tissue culture cells. The Proceedings of the National Academy of Sciences USA 92, 10104–10108. https://doi:10.1073/pnas.92.22.10104

Tong SY, Ki KD, Lee JM, Kang MJ, Ha TK, Chung SI, Chi SG, Lee SK. 2010. Frequent inactivation of hSRBC in ovarian cancers by promoter CpG island hypermethylation.  Acta Obstetricia et Gynecologica 89, 629–635. https://doi.org/10.3109/00016341003678443

Tran YK, Newsham IF. 1996. High-density marker analysis of 11p15.5 in non-small cell lung carcinomas reveals allelic deletion of one shared and one distinct region when compared to breast carcinomas. Cancer Research 56, 2916–2921.

Xu XL, Wu LC, Du F, Davis A, Peyton M, Tomizawa Y, Maitra A, Tomlinson G, Gazdar AF, Weissman BE, Bowcock AM, Baer R, Minna JD. 2001. Inactivation of human SRBC, located within the 11p15.5-p15.4 tumor suppressor region, in breast and lung cancers. Cancer Research 61, 7943–7949.

Zhao B, Bepler G. 2001. Transcript map and complete genomic sequence for the 310 kb region of minimal allele loss on chromosome segment 11p15.5 in non-small-cell lung cancer. Oncogene 20, 8154–8164. https://doi.org/10.1038/sj.onc.1205027

Zöchbauer-Müller S, Fong KM, Geradts J, Xu X, Seidl S, End-Pfützenreuter A, Lang G, Heller G, Zielinski CC, Gazdar AF, Minna JD. 2005. Expression of the candidate tumor suppressor gene hSRBC is frequently lost in primary lung cancers with and without DNA methylation. Oncogene 24, 6249–6255. https://doi.org/10.1038/sj.onc.1208775