RANKL triggers resistance to TRAIL-induced cell death in oral squamous cell carcinoma

Purushoth Ethiraj; Yuvaraj Sambam; Jessica D. Hathaway-SchraderAzizul HaqueChad M. NovinceSakamuri V. Reddy

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RANKL triggers resistance to TRAIL-induced cell death in oral squamous cell carcinoma

机译：抵抗TRAIL-induced细胞RANKL触发器死亡在口腔鳞状细胞癌

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Oral squamous cell carcinoma (OSCC) occurs as a malignancy of the oral cavity. RANK ligand (RANKL) is essential for osteoclast formation/bone resorption. Recently, we showed autoregulation of receptor activator of nuclear factor-kB ligand (RANKL) stimulates OSCC cell proliferation. OSCC cells show resistance to tumor necrosis factor related apoptosis inducing ligand (TRAIL) treatment. Therefore, we hypothesize that RANKL promotes resistance for TRAIL induction of OSCC apoptotic cell death. In this study, SCC14A and SCC74A cells cultured with TRAIL revealed high-level expression of RANKL which increased resistance to TRAIL inhibition of tumor cell proliferation. RANKL stimulation inhibited terminal deoxynucleotidyl transferase dUTP nick end labeling positive staining in TRAIL-treated cells. CRISPR/Cas-9 knockout of RANKL (RANKL-KO) increased caspase-9, caspase-3 activity and cytochrome c release in OSCC cells. RANKL inhibited proapoptotic proteins BAD and BAX expression. TRAIL treatment suppressed the SQSTMl/p62 and RANKL restored the expression. Interestingly, RANKL alone significantly increased proteasome activity. RANKL-KO in OSCC cells inhibited autophagic activity as evidenced by decreased light chain 3B-II and beclin-1 expression. Thus, RANKL stimulation of OSCC tumor cells triggered resistance for TRAIL-induced OSCC cell death. Taken together, blockade of RANKL may inhibit OSCC tumor progression and enhance the potential of TRAIL induced OSCC tumor cell apoptosis.

机译：口腔鳞状细胞癌(OSCC)发生口腔恶性肿瘤。(RANKL)对破骨细胞至关重要形成/骨吸收。自动调整的核受体激活factor-kB配体(RANKL)刺激OSCC细胞扩散。肿瘤坏死因子相关的凋亡诱导配体(TRAIL)治疗。假设RANKL促进阻力TRAIL诱导OSCC凋亡细胞死亡。这项研究中,SCC14A SCC74A细胞培养跟踪显示高级RANKL的表达增加抵抗TRAIL抑制肿瘤细胞增殖。抑制末端转移酶dUTP尼克结束标记阳性染色TRAIL-treated细胞。在OSCC细胞活性和细胞色素c的释放。RANKL抑制proapoptotic蛋白质坏和伯灵顿表达式。SQSTMl / p62和RANKL恢复了表情。有趣的是,RANKL显著蛋白酶体活性增加。细胞抑制自噬活动就是明证通过减少轻链3 b-ii和beclin-1表达式。细胞触发电阻TRAIL-induced OSCC细胞死亡。抑制OSCC肿瘤发展和提高小道OSCC诱导肿瘤细胞的潜力细胞凋亡。

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来源
《Journal of cellular physiology.》 |2020年第2期|1663-1673|共11页
作者
Purushoth Ethiraj; Yuvaraj Sambam; Jessica D. Hathaway-SchraderAzizul HaqueChad M. NovinceSakamuri V. Reddy;
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Department of Pediatrics, Medical University of South Carolina, Charleston, South Carolina;

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正文语种英语
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关键词
osteoclast differentiation factor; TNF-Related Apoptosis-Inducing Ligand; AutophagyCell Deathbone structureApoptosis;

机译：破骨细胞分化因子;TNF-Related凋亡诱导配体;AutophagyCell DeathbonestructureApoptosis;

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机译：Adu; Aged;; Aged, 80 and over;; Cadherins;; Carcinoma, Squamous Cell;; Cell Nucleus;; Cytoplasm;; Female;; Humans;; Laryngeal Neoplasms;; Male;; Middle Aged;; Neoplasm Staging;; Protein-Serine-Threonine Kinases;; Proto-Oncogene Proteins c-akt;; Retrospective Studies;; beta Catenin;; *成年人;; 老年人;; 老年人, 80以上;; 钙粘着糖蛋白类;; 癌, 鳞状细胞;; 细胞核;; 细胞质;; 喉肿瘤;; 肿瘤分期;; 蛋白质丝氨酸苏氨酸激酶;; 回顾性研究
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RANKL triggers resistance to TRAIL-induced cell death in oral squamous cell carcinoma

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