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학술저널
저자정보
Zhengbo Hu (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Lugen Li (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Wenxing Lan (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Xiao Wei (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Xiangyuan Wen (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Penghuan Wu (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Xianliao Zhang (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Xinhua Xi (The Affiliated Yuebei People’s Hospital of Shantou University Medical College Guangdong China) Yufa Li (The Second School of Clinical Medicine Southern Medical University Guangzhou China) Liqi Wu (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Wenhu Li (Shaoguan First People’s Hospital Affiliated to Southern Medical University Guangzhou China) Xiaohong Liao (University of Chinese Academy of Social Sciences (Graduate School) Guangzhou China)
저널정보
대한암학회 Cancer Research and Treatment Cancer Research and Treatment 제54권 제1호
발행연도
2022.1
수록면
277 - 293 (17page)
DOI
10.4143/crt.2021.320

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Purpose Osteosarcoma (OS) universally exhibits heterogeneity and cisplatin (CDDP) resistance. Although the Wee1/CDC2 and nuclear factor кB (NF-κB) pathways were reported to show abnormal activation in some tumor cells with CDDP resistance, whether there is any concrete connection is currently unclear. We explored it in human OS cells.Materials and Methods Multiple OS cell lines were exposed to a Wee1 inhibitor (AZD1775) and CDDP to assess the half-maximal inhibitory concentration values. Western blot, coimmunoprecipitation, confocal immunofluorescence, cell cycle, and Cell Counting Kit-8assays were performed to explore the connection between the Wee1/CDC2 and NF-κB pathways and their subsequent physiological contribution to CDDP resistance. Finally, CDDP-resistant PDX-OS xenograft models were established to confirm that AZD1775 restores the antitumor effects of CDDP.Results A sensitivity hierarchy of OS cells to CDDP and AZD1775 exists. In the highly CDDP-tolerant cell lines, Wee1 and RelA were physically crosslinked, which resulted in increased abundance of phosphorylated CDC2 (Y15) and RelA (S536) and consequent modulation of cell cycle progression, survival, and proliferation. Wee1 inhibition restored the effects of CDDP on these processes in CDDP-resistant OS cells. In addition, animal experiments with CDDP-resistant PDX-OS cells showed that AZD1775 combined with CDDP not only restored CDDP efficacy but also amplified AZD1775 in inhibiting tumor growth and prolonged the median survival of the mice.Conclusion Simultaneous enrichment of molecules in the Wee1/CDC2 and NF-κB pathways and their consequent coactivation is a new molecular mechanism of CDDP resistance in OS cells. OS with this molecular signature may respond well to Wee1 inhibition as an alternative treatment strategy.
#Osteosarcoma #CDDP resistance #Wee1 #RelA/NF-κB #PDX

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