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논문 기본 정보

자료유형
학술저널
저자정보
Kala Bonner (Department of Biological Sciences Tennessee State University Nashville TN USA) Danielle Borlay (Department of Biological Sciences Tennessee State University Nashville TN USA) Orica Kutten (Department of Biological Sciences Tennessee State University Nashville TN USA) Quincy A. Quick (Department of Biological Sciences Tennessee State University Nashville TN USA)
저널정보
대한뇌종양학회 Brain Tumor Research and Treatment Brain Tumor Research and Treatment Vol.8 No.1
발행연도
2020.1
수록면
43 - 52 (10page)

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Background: Microtubule actin crosslinking factor 1 (MACF1) is a spectraplakin cytoskeletal crosslinking protein whose function and role in cancer biology has lacked investigation. Recent studies have identified MACF1 as a novel target in glioblastomas expressed in tissue from tumor patient explants but not normal brain tissue and when silenced has an antitumorigenic impact on these tumors. Radiation as a single agent therapy to treat glioblastomas has been used for decades and has done little to improve survival of individuals diagnosed with this disease. However, contemporary clinical radiotherapy protocols have provided evidence that combinatorial radiotherapy approaches confer a therapeutic benefit in glioblastoma patients. In this study MACF1 was investigated as a radiosensitization target in glioblastomas. Methods: To provide context of MACF1 in glioblastomas, The Cancer Genome Atlas expression analyses were performed in conjunction with genes associated with glioblastoma evolution, while a genetic inhibitory approach, cell migratory assays, and immunofluorescence procedures were used to evaluate responses to MACF1 suppression with radiation. Additionally, expression analyses were conducted to assess co-expression of mTOR signaling pathway regulators and MACF1 in glioblastoma patient samples Results: Our amalgamation approach demonstrated that negative regulation of MACF1, which was positively correlated with epidermal growth factor receptor and p70s6k expression, enhanced the sensitivity of glioblastoma cells to radiation as a consequence of reducing glioblastoma cell viability and migration. Mechanistically, the antitumorigenic effects on glioblastoma cell behaviors after radiation and impairing MACF1 function were associated with decreased expression of ribosomal protein S6, a downstream effector of p70s6k. Conclusion: MACF1 represents a diagnostic marker with target specificity in glioblastomas that can enhance the efficacy of radiation while minimizing normal tissue toxicity. This approach could potentially expand combinatorial radiation strategies for glioblastoma treatments via impairment of translational regulatory processes that contribute to poor patient survival.
#MACF1 #Glioblastoma #Radiation #Ribosomal protein S6

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참고문헌 (39)

참고문헌 신청
Bernier G / 1996 / Cloning and characterization of mouse ACF7, a novel member of the dystonin subfamily of actin binding proteins / Genomics 38:19~29 google schola Ka M / 2014 / MACF1 regulates the migration of pyramidal neurons via microtubule dynamics and GSK-3 signaling / Dev Biol 395:4~18 google schola Lifang Hu / 2015 / Knockdown of microtubule actin crosslinking factor 1 inhibits cell proliferation in MC3T3-E1 osteoblastic cells / BMB Reports 48(10):583~588 google schola Afghani N / 2017 / Microtubule actin cross-linking factor 1, a novel target in glioblastoma / Int J Oncol 50:310~316 google schola Arai E / 2014 / Multilayer-omics analysis of renal cell carcinoma, including the whole exome, methylome and transcriptome / Int J Cancer 135:1330~1342 google schola

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