Angiomotin (AMOT) is a membrane protein that is aberrantly expressed in a variety of solid tumors. Accumulating evidence support that AMOT is involved in the pathological processes of tumor proliferation, apoptosis, and invasion. However, the potential role of AMOT in the pathogenesis of diffuse large B-cell lymphoma (DLBCL) remains elusive. In the present study, we investigated the expression level and biological function of AMOT in DLBCL. AMOT expression was significantly reduced in DLBCL biopsy section, and low AMOT expression was associated with poor clinical prognosis. Overexpression of AMOT by lentivirus in human DLBCL cells induced cell viability inhibition concomitant with an increased percentage of cells in G1 phase and decreased percentage in S phase. Moreover, AMOT upregulation increased the sensitivity of DLBCL cells to doxorubicin. Furthermore, overexpression of AMOT led to reduced activation of key kinases for the DNA damage response (DDR). The above results indicated that AMOT acts as a tumor suppressor via inhibition of the DDR, thus reducing the viability while increasing the chemosensitivity in DLBCL. In summary, AMOT may be a novel potential target for DLBCL therapeutic intervention.

血管动蛋白 (AMOT) 是一种在多种实体瘤中异常表达的膜蛋白。越来越多的证据支持AMOT参与了肿瘤增殖、凋亡和侵袭的病理过程。然而，AMOT 在弥漫性大 B 细胞淋巴瘤 (DLBCL) 发病机制中的潜在作用仍然难以捉摸。在本研究中，我们研究了 AMOT 在 DLBCL 中的表达水平和生物学功能。DLBCL活检切片中AMOT表达显着降低，AMOT低表达与临床预后不良有关。慢病毒在人DLBCL细胞中过表达AMOT诱导细胞活力抑制，同时G1期细胞百分比增加，S期细胞百分比降低。此外，AMOT 上调增加了 DLBCL 细胞对阿霉素的敏感性。此外，AMOT 的过表达导致 DNA 损伤反应 (DDR) 的关键激酶的激活减少。上述结果表明，AMOT 通过抑制 DDR 发挥肿瘤抑制作用，从而降低 DLBCL 的活力，同时增加化学敏感性。总之，AMOT 可能是 DLBCL 治疗干预的一个新的潜在靶点。