FAM135B (family with sequence similarity 135, member B) is related to the progression of esophageal squamous cell carcinoma (ESCC). However, the role played by the gene in radiosensitivity remains unknown. Herein, we examined the relationship between FAM135B and radiosensitivity. According to the results, FAM135B is highly expressed in ESCC cells, and ESCC cells with high levels of FAM135B are resistant to irradiation. Silencing FAM135B inhibits colony formation capability and cell cycle protein expression (pP53, CDK1), promotes cell cycle arrest at the G2/M phase following irradiation. Moreover, transcriptome sequencing analysis demonstrates that FAM135B regulates downstream PI3K/Akt/mTOR signaling pathway, and western blot verifies the result. One of the mechanisms of increasing radiosensitivity by silencing FAM135B expression in ESCC cells may be achieved by regulating the PI3K/Akt/mTOR signaling pathway. Silencing FAM135B shows synergy with PI3K/Akt/mTOR pathway inhibitor (rapamycin) in increasing radiosensitivity, regulating the expression of cell cycle protein and inducing apoptosis of ESCC cells. The results indicate that FAM135B could be a potential treatment target for ESCC in management of radiosensitivity.

FAM135B（序列相似性为135的家庭，成员B）与食管鳞状细胞癌（ESCC）的进展有关。但是，该基因在放射敏感性中所起的作用仍然未知。在本文中，我们研究了FAM135B与放射敏感性之间的关系。根据结果​​，FAM135B在ESCC细胞中高表达，并且具有高水平的FAM135B的ESCC细胞具有抗辐射性。沉默FAM135B抑制集落形成能力和细胞周期蛋白表达（pP53，CDK1），促进辐射后G2 / M期的细胞周期停滞。此外，转录组测序分析表明，FAM135B调节下游PI3K / Akt / mTOR信号传导途径，并且Western blot验证了结果。通过沉默ESCC细胞中FAM135B表达来增加放射敏感性的机制之一可以通过调节PI3K / Akt / mTOR信号传导途径来实现。沉默的FAM135B在增加放射敏感性，调节细胞周期蛋白的表达并诱导ESCC细胞凋亡方面表现出与PI3K / Akt / mTOR途径抑制剂（雷帕霉素）的协同作用。结果表明，FAM135B可能是ESCC在放射敏感性管理中的潜在治疗靶标。