PDF(Pubmed)
Abstract：
BACKGROUND: Inhibitor of DNA Binding 2 (ID2) plays a crucial role in tumor cell proliferation, invasion, metastasis, and stemness. Aberrant ID2 expression is associated with poor prognosis in various cancers. However, the specific function of ID2 in thyroid cancer remain unclear.
METHODS: The TCGA database were utilized to explore the clinical relevance of ID2 in cancer. GO, KEGG, and TIMER were employed to predict the potential roles of ID2 in cancer. Functional analysis, including CCK-8, colony formation, transwell, wound healing, and sphere formation experiments, were conducted to determine the biological functions of ID2 in human cancers. Western blot (WB), RT-qPCR, and immunohistochemical (IHC) analyses were used to investigate the relationship between ID2 and downstream targets.
RESULTS: Our study revealed significant overexpression of ID2 in various malignant tumor cells. Knocking ID2 significantly inhibited cancer cell proliferation and invasion, while overexpressing ID2 enhanced these capabilities. Additionally, ID2 mediates resistance of cancer cells to protein kinase B (or Akt) inhibitions. Further WB and IHC experiments indicated that ID2 promotes the phosphorylation activation of phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway, thereby upregulating the expression of downstream proliferation, epithelial-mesenchymal transition (EMT), and stemness-related markers.
CONCLUSIONS: We found that ID2 significantly promotes thyroid cancer cell proliferation, migration, EMT, and stemness through the PI3K/Akt pathway. Moreover, ID2 plays a crucial role in regulating cancer immune responses. It may serve as a potential biomarker for enhancing the efficacy of chemotherapy, targeted therapy, and immunotherapy against cancer.
METHODS: The TCGA database were utilized to explore the clinical relevance of ID2 in cancer. GO, KEGG, and TIMER were employed to predict the potential roles of ID2 in cancer. Functional analysis, including CCK-8, colony formation, transwell, wound healing, and sphere formation experiments, were conducted to determine the biological functions of ID2 in human cancers. Western blot (WB), RT-qPCR, and immunohistochemical (IHC) analyses were used to investigate the relationship between ID2 and downstream targets.
RESULTS: Our study revealed significant overexpression of ID2 in various malignant tumor cells. Knocking ID2 significantly inhibited cancer cell proliferation and invasion, while overexpressing ID2 enhanced these capabilities. Additionally, ID2 mediates resistance of cancer cells to protein kinase B (or Akt) inhibitions. Further WB and IHC experiments indicated that ID2 promotes the phosphorylation activation of phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway, thereby upregulating the expression of downstream proliferation, epithelial-mesenchymal transition (EMT), and stemness-related markers.
CONCLUSIONS: We found that ID2 significantly promotes thyroid cancer cell proliferation, migration, EMT, and stemness through the PI3K/Akt pathway. Moreover, ID2 plays a crucial role in regulating cancer immune responses. It may serve as a potential biomarker for enhancing the efficacy of chemotherapy, targeted therapy, and immunotherapy against cancer.
摘要：
背景：DNA结合抑制剂2（ID2）在肿瘤细胞增殖中起着至关重要的作用，入侵,转移,和干劲。在各种癌症中,异常的ID2表达与不良预后相关。然而,ID2在甲状腺癌中的具体功能尚不清楚.
方法：利用TCGA数据库探讨ID2在癌症中的临床意义。GO,KEGG,和TIMER用于预测ID2在癌症中的潜在作用。功能分析,包括CCK-8，集落形成，transwell,伤口愈合，和球体形成实验，进行以确定ID2在人类癌症中的生物学功能。Westernblot(WB),RT-qPCR,和免疫组织化学（IHC）分析用于研究ID2和下游靶标之间的关系。
结果：我们的研究显示ID2在各种恶性肿瘤细胞中显著过表达。敲除ID2显著抑制癌细胞增殖和侵袭,而过度表达ID2增强了这些能力。此外,ID2介导癌细胞对蛋白激酶B(或Akt)抑制的抗性。进一步的WB和IHC实验表明ID2促进磷脂酰肌醇3-激酶(PI3K)/Akt信号通路的磷酸化激活,从而上调下游增殖的表达，上皮-间质转化（EMT），和干性相关标记。
结论：我们发现ID2显著促进甲状腺癌细胞增殖，迁移,EMT,和通过PI3K/Akt途径的干性。此外，ID2在调节癌症免疫应答中起着至关重要的作用。它可以作为增强化疗疗效的潜在生物标志物，靶向治疗,和针对癌症的免疫疗法。
方法：利用TCGA数据库探讨ID2在癌症中的临床意义。GO,KEGG,和TIMER用于预测ID2在癌症中的潜在作用。功能分析,包括CCK-8，集落形成，transwell,伤口愈合，和球体形成实验，进行以确定ID2在人类癌症中的生物学功能。Westernblot(WB),RT-qPCR,和免疫组织化学（IHC）分析用于研究ID2和下游靶标之间的关系。
结果：我们的研究显示ID2在各种恶性肿瘤细胞中显著过表达。敲除ID2显著抑制癌细胞增殖和侵袭,而过度表达ID2增强了这些能力。此外,ID2介导癌细胞对蛋白激酶B(或Akt)抑制的抗性。进一步的WB和IHC实验表明ID2促进磷脂酰肌醇3-激酶(PI3K)/Akt信号通路的磷酸化激活,从而上调下游增殖的表达，上皮-间质转化（EMT），和干性相关标记。
结论：我们发现ID2显著促进甲状腺癌细胞增殖，迁移,EMT,和通过PI3K/Akt途径的干性。此外，ID2在调节癌症免疫应答中起着至关重要的作用。它可以作为增强化疗疗效的潜在生物标志物，靶向治疗,和针对癌症的免疫疗法。
