Abstract

Purpose

Although radiotherapy is a common treatment option for all kinds of cancer patients, including ovarian cancer, a major obstacle limiting its application in the development of resistance. Therefore, it is urgently needed to clarify the mechanism of radiosensitivity modulation.

Materials and methods

We obtained open datasets and analyzed the expression of collagen type XI alpha 1 (COL11A1) in ovarian cancer patients with different stages. Meanwhile, the correlation of COL11A1 and survival outcomes is determined by Kaplan–Meier analysis. The role of COL11A1 in cell proliferation was observed in an in vitro knockdown system. SKOV3 radioresistant cells were established to determine the role of COL11A1 on radioresistant in ovarian cancer.

Results and discussion

COL11A1 were highly enriched in late-stage ovarian cancer tumor tissues and negatively correlated with survival outcomes in ovarian cancer. The functional analysis found that COL11A1 promoted ovarian cancer cell proliferation in vitro. Importantly, COL11A1 decreased radiosensitivity in ovarian cancer by AKT activation. Paired related homeobox 1 (PRRX1) acted as an upstream transcription factor to regulate COL11A1 expression in ovarian cancer. Increased COL11A1 expression is related to low survival outcomes and radiosensitivity in ovarian cancer.

Conclusions

Targeting COL11A1 is a promising strategy for improving radiotherapy efficiency.

中文翻译：

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PRRX1激活COL11A1促进卵巢癌的肿瘤进展和放射抗性

摘要

目的

尽管放疗是包括卵巢癌在内的各种癌症患者的常见治疗选择，但这是限制其在耐药性发展中应用的主要障碍。因此，迫切需要阐明放射敏感性调节的机制。

材料和方法

我们获得了开放数据集并分析了不同阶段卵巢癌患者中 XI α 1 型胶原蛋白 (COL11A1) 的表达。同时，COL11A1 与生存结果的相关性由 Kaplan-Meier 分析确定。在体外敲低系统中观察到 COL11A1 在细胞增殖中的作用。建立SKOV3抗辐射细胞以确定COL11A1在卵巢癌抗辐射中的作用。

结果和讨论

COL11A1在晚期卵巢癌肿瘤组织中高度富集，与卵巢癌的生存结果呈负相关。功能分析发现COL11A1在体外促进卵巢癌细胞增殖。重要的是，COL11A1 通过 AKT 激活降低了卵巢癌的放射敏感性。配对相关同源框 1 (PRRX1) 作为上游转录因子调节卵巢癌中的 COL11A1 表达。COL11A1 表达增加与卵巢癌的低生存结果和放射敏感性有关。

结论

靶向 COL11A1 是提高放疗效率的一种很有前景的策略。