Chitinase 3 like-1 (CHI3L1) has been reported to function as an oncogene in many types of cancer. However, the biological function of CHI3L1 in nasopharyngeal carcinoma (NPC) remains unknown. Differentially expressed genes (DEGs) in NPC tissues in GSE64634 and GSE12452 were downloaded from Gene Expression Omnibus (GEO). CHI3L1, interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) mRNA expression was examined by qRT-PCR. Cell proliferation was evaluated by CCK-8 and EdU incorporation assays. Western blot analysis was used to measure the changes of CHI3L1, nuclear factor-κappaB (NF-κB), and protein kinase B (Akt) pathways. Gene ontology (GO) enrichment and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analyses were performed using DAVID database. We identified 3 overlapping DEGs using Draw Venn diagram, among which CHI3L1 was chosen for the following analyses. CHI3L1 was upregulated in NPC tissues and cells. CHI3L1 silencing suppressed inflammatory response by inactivating the NF-κB pathway and inhibited cell proliferation in NPC cells. On the contrary, CHI3L1 overexpression induced inflammatory response by activating the NF-κB pathway and promoted cell proliferation in NPC cells. According to GO and KEGG analyses, CHI3L1 positive regulates Akt signaling and is enriched in the PI3K-Akt pathway. CHI3L1 knockdown inhibited the Akt pathway, and CHI3L1 overexpression activated the Akt pathway in NPC cells. Akt overexpression abolished the effects of CHI3L1 knockdown on inflammatory response, NF-κB pathway, and proliferation in NPC cells. On the contrary, Akt knockdown abolished the effects of CHI3L1 overexpression on inflammatory response, NF-κB pathway, and proliferation in NPC cells. CHI3L1 knockdown inhibited NF-κB-dependent inflammatory response and promoting proliferation in NPC cells by inactivating the Akt pathway.

中文翻译：

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Chitinase 3 like-1激活Akt通路，诱导NF-κB依赖性促炎细胞因子的释放，促进鼻咽癌细胞的增殖能力


据报道，几丁质酶 3 like-1 (CHI3L1) 在许多类型的癌症中充当癌基因。然而，CHI3L1 在鼻咽癌（NPC）中的生物学功能仍不清楚。从 Gene Expression Omnibus (GEO) 下载 GSE64634 和 GSE12452 中鼻咽癌组织中的差异表达基因 (DEG)。通过 qRT-PCR 检查 CHI3L1、白细胞介素 6 (IL-6) 和肿瘤坏死因子 α (TNF-α) mRNA 表达。通过 CCK-8 和 EdU 掺入测定评估细胞增殖。 Western blot分析用于测量CHI3L1、核因子-κappaB (NF-κB)和蛋白激酶B (Akt)通路的变化。使用 DAVID 数据库进行基因本体（GO）富集和京都基因和基因组百科全书（KEGG）通路分析。我们使用Draw Venn图识别了3个重叠的DEG，其中选择CHI3L1进行以下分析。 CHI3L1 在鼻咽癌组织和细胞中表达上调。 CHI3L1 沉默通过灭活 NF-κB 通路来抑制炎症反应，并抑制鼻咽癌细胞中的细胞增殖。相反，CHI3L1过表达通过激活NF-κB通路诱导炎症反应，促进鼻咽癌细胞增殖。根据 GO 和 KEGG 分析，CHI3L1 正向调节 Akt 信号传导，并在 PI3K-Akt 通路中富集。 CHI3L1 敲低抑制 Akt 通路，CHI3L1 过表达激活 NPC 细胞中的 Akt 通路。 Akt 过表达消除了 CHI3L1 敲低对鼻咽癌细胞炎症反应、NF-κB 通路和增殖的影响。相反，Akt 敲低消除了 CHI3L1 过表达对鼻咽癌细胞炎症反应、NF-κB 通路和增殖的影响。 CHI3L1 敲低可抑制 NF-κB 依赖性炎症反应，并通过失活 Akt 通路促进 NPC 细胞增殖。