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Overexpression of the thymosin β-10 gene in human ovarian cancer cells disrupts F-actin stress fiber and leads to apoptosis

A Corrigendum to this article was published on 13 August 2002

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Abstract

To understand the molecular changes during ovarian cancer development, we profiled differentially expressed genes in five paired normal and cancerous ovarian tissues. Among the genes that showed differential expression, thymosin β-10 expression was decreased in four of five cancer tissues. The decreased level of expression was confirmed by Northern. To investigate the gene's functional role in ovarian cancers, we constructed an adenovirus vector expressing thymosin β-10 and used it to infect ovarian cancer cell lines PA-I and SKOV3. The infected cells showed disrupted F-actin stress fibers, markedly decreased cell growth, and a high rate of apoptosis. Thus, because loss of thymosin β-10 expression may contribute to the development of a subset of ovarian cancers, restoration of thymosin β-10 expression may be a new strategy for ovarian cancer treatment.

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References

  • Bao L, Loda M, Janmey PA, Stewart R, Anand-Apte B, Zetter BR . 1996 Nat. Med. 2: 1322–1328

  • Caduff RF, Svoboda-Newman SM, Ferguson AW, Jonston CM, Frank TS . 1999 Am. J. Surg. Pathol. 23: 323–328

  • Carpintero P, Franco del Amo F, Anadon R, Gomez-Marquez J . 1996 FEBS Lett. 394: 103–106

  • DeRisi J, Penland L, Brown PO, Bittner ML, Meltzer PS, Ray M, Chen Y, Su YA, Trent JM . 1996 Nat. Genet. 14: 457–460

  • Eadie JS, Kim SW, Allen PG, Hutchinson LM, Kantor JD, Zetter BR . 2000 J. Cell. Biochem. 77: 277–287

  • Fuller GN, Rhee CH, Hess KR, Caskey LS, Wang R, Bruner JM, Alfred Yung WK, Zhang W . 1999 Cancer Res. 59: 4228–4232

  • Gold JS, Bao L, Ghoussoub RA, Zetter BR, Rimm DL . 1997 Mod. Pathol. 10: 1106–1112

  • Hall AK, Hempstead J, Morgan JI . 1990 Mol. Brain Res. 8: 129–135

  • Hall AK, Aten R, Behrman HR . 1991 Mol. Cell. Endocrinol. 79: 37–41

  • Hall AK . 1994a Ren Fail 16: 243–254

  • Hall AK . 1994b Med. Hypotheses. 43: 125–131

  • Hall AK . 1995 Cell. Mol. Biol. Res. 41: 167–180

  • Henriksen R, Strang P, Wilander E, Bδckstrωm T, Tribukait B, Oberg K . 1994 Gynecol. Oncol. 53: 301–306

  • Hough CD, Sherman-Baust CA, Pizer ES, Montz FJ, Im DD, Rosenshein NB, Cho KR, Riggins GJ, Morin PJ . 2000 Cancer Res. 60: 6281–6287

  • Huang P, Feng L, Oldham EA, Keating MJ, Plunkett W . 2000 Nature 407: 390–395

  • Iguchi K, Hamatake M, Ishida R, Usami Y, Adachi T, Yamamoto H, Koshida K, Uchibayashi T, Hirano K . 1998 Eur. J. Biochem. 253: 766–770

  • Marian AJW, Goos NPV, Dirk JR, Henri PJB . 1993 Int. J. Cancer 53: 278–284

  • Marx D, Binder C, Meden H, Lenthe T, Ziemek T, Hiddemann T, Kuhn W, Schauer A . 1997 Anticancer Res. 17: 2233–2240

  • Meden H, Marx D, Raab T, Krohn M, Schauer A, Kuhn W . 1995 J. Obstet. Gynaecol. 21: 167–178

  • Morita K, Ono Y, Fukui H, Tomita S, Ueda Y, Terano A, Fujimori T . 2000 Pathol Int. 50: 219–223

  • Nachmias VT . 1993 Curr. Opin. Cell. Biol. 5: 56–62

  • NIH Consensus Statement . 1994 12: 1–30

  • Pollard TD, Cooper JA . 1986 Ann. Rev. Biochem. 55: 987–1035

  • Rauh-Adelmann C, Lau KM, Sabeti N, Long JP, Mok SC, Ho SM . 2000 Mol. Carcinog. 28: 236–246

  • Santelli G, Califano D, Chiappetta G, Vento MT, Bartoli PC, Zullo F, Trapasso F, Viglietto G, Fusco A . 1999 Am. J. Pathol. 155: 799–804

  • Velculescu VE, Zhang L, Vogelstein B, Kinzler KW . 1995 Science 170: 484–487

  • Verghese-Nikolakaki S, Apostolikas N, Livaniou E, Ithakissios DS, Evangelatos GP . 1996 Br. J. Cancer 74: 1441–1444

  • Yamamoto T, Gotoh M, Kitajima M, Hirohashi S . 1993 Biochem. Biophys. Res. Commun. 193: 706–710

  • Yu FX, Lin SC, Morrison-Bogorad M, Atkinson MA, Yin HL . 1993 J. Biol. Chem. 268: 502–509

  • Yu FX, Lin SC, Morrison-Bogorad M, Yin HL . 1994 Cell. Motil. Cytoskeleton. 27: 13–25

  • Zhang L, Zhou W, Velculescu VE, Kern SE, Hruban RH, Hamilton SR, Vogelstein B, Kinzler KW . 1997 Science 276: 1268–1272

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Acknowledgements

This work was partially supported by G7 and SRC funds of the Korea Science and Engineering Foundation and by Texas Tobacco Settlement Funds appropriated by the Texas Legislature to The University of Texas M. D. Anderson Cancer Center.

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Correspondence to Je-Ho Lee.

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Lee, SH., Zhang, W., Choi, JJ. et al. Overexpression of the thymosin β-10 gene in human ovarian cancer cells disrupts F-actin stress fiber and leads to apoptosis. Oncogene 20, 6700–6706 (2001). https://doi.org/10.1038/sj.onc.1204683

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