Unità di Medicina Traslazionale per la Salute della Donna e del Bambino, Dipartimento Scienze della Salute della Donna, del Bambino e di Sanità Pubblica, Fondazione Policlinico Universitario A. Gemelli, IRCCS, Roma, Italia.
Dipartimento Universitario Scienze della Vita e Sanità Pubblica - Sezione di Ginecologia ed Ostetricia - Università Cattolica del Sacro Cuore, Roma, Italia.
Cell Death Dis. 2021 Oct 12;12(10):933. doi: 10.1038/s41419-021-04229-y.
Cervical cancer (CC) is the fourth most common cause of cancer-related death in women. According to international guidelines, a standard treatment for locally advanced cervical cancer (LACC) consists of exclusive concurrent chemoradiation treatment (CRT). However, chemoradioresistance and subsequent relapse and metastasis of cancer occur in many patients, and survival for these women has generally remained poor. Therefore, strategies to overcome resistance are urgently needed. We have recently reported a radiosensitizing effect of the signal transducer and activator of transcription 1 (STAT1) in CC, associated with the control of [Poly(ADP-ribose) polymerase -1] PARP1 levels, a key factor in cell response to DNA damage induced by radiation. Here, we sought to decipher the underlying mechanism of STAT1-mediated control of PARP1, elucidating its role as a radiosensitizer in CC. Functional and molecular biology studies demonstrated that STAT1 may act at both transcriptional and posttranscriptional levels to modulate PARP1 expression in CC cells. In light of these results, we tested the effect of Olaparib in sensitizing CC cells to radiation and investigated signaling pathways involved in the activity observed. Results showed that PARP1 inhibition, at clinically achievable doses, may indeed selectively improve the sensitivity of resistant CC cells to DNA-damaging treatment. The translational relevance of our findings was supported by preliminary results in a limited patient cohort, confirming that higher PARP1 levels are significantly associated with a radioresistant phenotype. Finally, bioinformatics analysis of GEPIA and TCGA databases, demonstrated that PARP1 mRNA is higher in CC than in normal tissues and that increased PARP1 mRNA expression levels are associated with poor prognosis of LACC patients. Overall, our data open new opportunities for the development of personalized treatments in women diagnosed with CC.
宫颈癌(CC)是女性癌症相关死亡的第四大主要原因。根据国际指南,局部晚期宫颈癌(LACC)的标准治疗方法包括单纯同步放化疗(CRT)。然而,许多患者存在化疗和放疗耐药,随后癌症复发和转移,这些女性的生存状况普遍较差。因此,迫切需要寻找克服耐药的策略。我们最近报道了信号转导子和转录激活子 1(STAT1)在宫颈癌中具有放射增敏作用,这与[多聚(ADP-核糖)聚合酶-1]PARP1 水平的控制有关,PARP1 是细胞对辐射诱导的 DNA 损伤做出反应的关键因素。在这里,我们试图阐明 STAT1 介导的 PARP1 调控的潜在机制,阐明其在宫颈癌中作为放射增敏剂的作用。功能和分子生物学研究表明,STAT1 可能在转录和转录后水平上作用,以调节宫颈癌细胞中 PARP1 的表达。鉴于这些结果,我们测试了奥拉帕利在使宫颈癌细胞对辐射敏感方面的作用,并研究了所观察到的活性涉及的信号通路。结果表明,PARP1 抑制剂在临床可达到的剂量下确实可以选择性地提高耐药宫颈癌细胞对 DNA 损伤治疗的敏感性。在一个有限的患者队列中进行的初步结果支持了我们研究结果的转化相关性,证实较高的 PARP1 水平与放射抗拒表型显著相关。最后,GEPIA 和 TCGA 数据库的生物信息学分析表明,PARP1 mRNA 在宫颈癌中高于正常组织,并且 PARP1 mRNA 表达水平的增加与 LACC 患者的不良预后相关。总体而言,我们的数据为患有宫颈癌的女性开发个性化治疗方法提供了新的机会。