Department of Obstetrics and Gynecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China; Department of Orthopaedic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Sarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Gynecol Oncol. 2018 Jul;150(1):143-150. doi: 10.1016/j.ygyno.2018.04.557. Epub 2018 Apr 24.
Multidrug resistance is the major cause of treatment failure in ovarian cancer. p62 (SQSTM1) is a multifunctional protein involved in multiple cellular processes including proliferation, drug sensitivity and autophagy-associated cancer cell growth. However, the role of p62 in drug resistance remains controversial.
In this study, we examined p62 expression by immunohistochemistry in a unique ovarian cancer tissue microarray (TMA), which was constructed with paired primary, metastatic, and recurrent tumor tissues. The expression levels of p62 and autophagy related proteins were evaluated in two panels of human cancer cell lines by western blot. Cell viabilities were determined by MTT assay after exposure ovarian cancer cells to different concentrations of paclitaxel alone or in combination with autophagy inhibitors.
Both the metastatic and recurrent tumor tissues expressed less p62 than the patient-matched primary tumor. A significant inverse correlation has been found between p62 expression and both the disease-free survival and overall survival. Additionally, multidrug resistant cancer cell lines expressed lower levels of p62 as compared with their parental drug sensitive cell lines. Importantly, inhibition of autophagy enhanced paclitaxel sensitivity in drug resistant ovarian cancer cells. Furthermore, the wound healing assay exhibited that the inhibition of autophagy significantly decreased resistant ovarian cancer cell migration in vitro.
Our findings highlight the potential of p62 as a new prognostic marker for ovarian cancer patients and p62's associated autophagy pathway may be a promising therapeutic target to prevent metastasis, recurrence and to reverse drug resistance in ovarian cancer.
多药耐药是卵巢癌治疗失败的主要原因。p62(SQSTM1)是一种多功能蛋白,参与多种细胞过程,包括增殖、药物敏感性和自噬相关的癌细胞生长。然而,p62 在耐药性中的作用仍存在争议。
在这项研究中,我们通过免疫组织化学在独特的卵巢癌组织微阵列(TMA)中检查了 p62 的表达,该 TMA 是由配对的原发性、转移性和复发性肿瘤组织构建的。通过 Western blot 评估了两个人类癌细胞系面板中 p62 和自噬相关蛋白的表达水平。在单独或与自噬抑制剂联合使用紫杉醇处理卵巢癌细胞后,通过 MTT 测定法确定细胞活力。
转移性和复发性肿瘤组织的 p62 表达均低于患者匹配的原发性肿瘤。p62 表达与无病生存期和总生存期之间存在显著的负相关。此外,多药耐药癌细胞系的 p62 表达水平低于其亲本药物敏感细胞系。重要的是,自噬抑制增强了耐药性卵巢癌细胞对紫杉醇的敏感性。此外,划痕愈合试验表明,自噬抑制显著降低了体外耐药性卵巢癌细胞的迁移。
我们的研究结果强调了 p62 作为卵巢癌患者新的预后标志物的潜力,并且 p62 相关的自噬途径可能是预防转移、复发和逆转卵巢癌耐药性的有前途的治疗靶点。