1. 細胞的基礎信息

2. 細胞常見的研究有哪些？

a) 研究腫瘤細胞的生物學特性

b) 藥物篩選及癌癥治療的研發

c) 癌變機理研究及抗癌藥篩選檢測

d) 建立細胞模型

3. 細胞相關的文獻有哪些？

[1]王昆鋒,陳功,丁潔.丙泊酚對人神經膠質母細胞瘤（U343）活性、凋亡、侵襲和轉移能力的影響[J].醫學信息,2021,34(02):86-89.

（目的：探究丙泊酚對人神經膠質母細胞瘤(U343)活性、凋亡、侵襲和轉移能力的影響。方法：將處于對數生長期的人神經膠質母細胞瘤(U343)隨機分為4組，分別為N組、S2組(Propofol 2μmol/L)、S5組(Propofol 5μmol/L)及S10組(Propofol10μmol/L)。除N組外，其余實驗組加入相應濃度的丙泊酚，四組均在常氧培養箱培養48 h,采用CCK-8法檢測神經膠質母細胞瘤(U343)活力，流式法檢測細胞的凋亡，劃痕實驗檢測細胞遷移能力，蛋白免疫印跡法檢測凋亡相關蛋白Caspase-3﹑細胞因子VEGF的表達量。結果：結果CCK-8檢測顯示，S2組、S5組及S10組OD值低于N組，差異有統計學意義(P<0.05)，且隨著丙泊酚濃度的升高細胞活力降低，OD值降低。流式檢測顯示，S2組、S5組及S10組細胞凋亡率和死亡率高于N組，差異有統計學意義(P<0.05)，且隨著培養皿中丙泊酚濃度的升高,細胞凋亡(早期凋亡+晚期凋亡)率和死亡率升高；劃痕實驗顯示：S2組、S5組及S10組遷移率低于N組，差異有統計學意義(P<0.05)，且隨著培養皿丙泊酚濃度升高，遷移能力降低;蛋白免疫印跡法顯示，S2組、S5組及S10組凋亡相關蛋白Caspase-3表達高于N組，VEGF蛋白表達低于N組,差異有統計學意義(P<0.05)。結論：丙泊酚能降低人神經膠質母細胞瘤(U343)的活力，增加細胞凋亡，抑制腫瘤細胞的增殖和遷移，且抑制程度10μmol/L>5μmol/L>2μmol/L。）

[2]Da Costa Almeida TL, Rodrigues AR, Cirino M, Trevisan FA, Peria F, Tirapelli D, Carlotti CG Jr. Modulation of Genes and MicroRNAs in the Neurospheres of Glioblastoma Cell Lines U343 and T98G Induced by Ionizing Radiation and Temozolomide Therapy. Cureus. 2022 Dec 5;14(12):e32211.

（Introduction: Glioblastoma is the most prevalent primary malignant neoplasm of the central nervous system. It has increased its incidence, while the overall survival remains over 14 months. Purpose: The purpose is to evaluate the expression of the genes EGFR, PTEN, MGMT, and IDH1/2, and microRNAs miR-181b, miR-145, miR-149, and miR-128a in adhered cells (AC) and neurospheres (NS) from cell lines (T98G and U343) submitted to temozolomide (TMZ) and ionizing radiation (IR). Methods: T98G and U343 were treated with TMZ, IR, and TMZ+IR. The analysis of gene expression and miRNAs was performed using real-time PCR. Results: This study demonstrated: a) an improvement in the expression of IDH1 after IR and TMZ + IR in the NS (T98G); b) an increase in the expression of MGMT in NS (T98G) in IR groups and TMZ + IR. The expression of miRNAs results as a) AC (U343) expressed more miR-181b after TMZ, IR, and TMZ + IR; and miR-128a improved after TMZ, IR, and TMZ + IR; b) NS (T98G) after TMZ + IR expressed: miR-181b; miR-149; miR-145 and miR-128a; c) NS (U343) after IR huge expressed miR-149 and miR-145. Conclusion:IR was an independent and determining radioresistance factor in NS. However, we observed no complementarity action of oncomiRs regulation.