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Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a Tsc2‑deficient cell line

  • Authors:
    • Takayuki Kitano
    • Keiko Nishikawa
    • Tetsuya Takagaki
    • Yoshinobu Sugitani
    • Okio Hino
    • Toshiyuki Kobayashi
  • View Affiliations / Copyright

    Affiliations: Department of Molecular Pathogenesis, Juntendo University Graduate School of Medicine, Tokyo 113‑8421, Japan, Department of Pathology and Oncology, Juntendo University Faculty of Medicine, Tokyo 113‑8421, Japan
    Copyright: © Kitano et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 315
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    Published online on: May 12, 2023
       https://doi.org/10.3892/etm.2023.12014
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Abstract

Tuberous sclerosis complex (TSC) is an intractable inherited disease caused by a germline mutation in either the TSC complex subunit 1 (TSC1) or TSC2 tumor suppressor genes. Recent progress in the treatment of TSC with rapamycin has provided benefits to patients with TSC. However, the complete elimination of tumors is difficult to achieve as regrowth often occurs after a drug is suspended; thus, more efficient medication and novel therapeutic targets are required. To overcome tumor remnants in the treatment of TSC, the present study investigated rapamycin‑responsive signaling pathways in Tsc2‑deficient tumor cells, focusing on heat shock protein‑related pathways. The expression levels of heat shock protein family B (small) member 1 (Hspb1; also known as HSP25/27) were increased by rapamycin treatment. The phosphorylation of Hspb1 was also increased. The knockdown of Hspb1 suppressed cell proliferation in the absence of rapamycin, and the overexpression of Hspb1 enhanced cell proliferation both in the presence and absence of rapamycin. Pathways associated with Hspb1 may present target candidates for treatment of TSC.
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Copy and paste a formatted citation
Spandidos Publications style
Kitano T, Nishikawa K, Takagaki T, Sugitani Y, Hino O and Kobayashi T: Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line. Exp Ther Med 26: 315, 2023.
APA
Kitano, T., Nishikawa, K., Takagaki, T., Sugitani, Y., Hino, O., & Kobayashi, T. (2023). Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line. Experimental and Therapeutic Medicine, 26, 315. https://doi.org/10.3892/etm.2023.12014
MLA
Kitano, T., Nishikawa, K., Takagaki, T., Sugitani, Y., Hino, O., Kobayashi, T."Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line". Experimental and Therapeutic Medicine 26.1 (2023): 315.
Chicago
Kitano, T., Nishikawa, K., Takagaki, T., Sugitani, Y., Hino, O., Kobayashi, T."Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line". Experimental and Therapeutic Medicine 26, no. 1 (2023): 315. https://doi.org/10.3892/etm.2023.12014
Copy and paste a formatted citation
x
Spandidos Publications style
Kitano T, Nishikawa K, Takagaki T, Sugitani Y, Hino O and Kobayashi T: Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line. Exp Ther Med 26: 315, 2023.
APA
Kitano, T., Nishikawa, K., Takagaki, T., Sugitani, Y., Hino, O., & Kobayashi, T. (2023). Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line. Experimental and Therapeutic Medicine, 26, 315. https://doi.org/10.3892/etm.2023.12014
MLA
Kitano, T., Nishikawa, K., Takagaki, T., Sugitani, Y., Hino, O., Kobayashi, T."Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line". Experimental and Therapeutic Medicine 26.1 (2023): 315.
Chicago
Kitano, T., Nishikawa, K., Takagaki, T., Sugitani, Y., Hino, O., Kobayashi, T."Induction by rapamycin and proliferation‑promoting activity of Hspb1 in a <em>Tsc2</em>‑deficient cell line". Experimental and Therapeutic Medicine 26, no. 1 (2023): 315. https://doi.org/10.3892/etm.2023.12014
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