1. 细胞的基础信息

2. 细胞常见的研究有哪些？

a) 研究肿瘤细胞的生物学特性

b) 药物筛选及癌症治疗的研发

c) 癌变机理研究及抗癌药筛选检测

d) 建立细胞模型

3. 细胞相关的文献有哪些？

[1]王昆锋,陈功,丁洁.丙泊酚对人神经胶质母细胞瘤（U343）活性、凋亡、侵袭和转移能力的影响[J].医学信息,2021,34(02):86-89.

（目的：探究丙泊酚对人神经胶质母细胞瘤(U343)活性、凋亡、侵袭和转移能力的影响。方法：将处于对数生长期的人神经胶质母细胞瘤(U343)随机分为4组，分别为N组、S2组(Propofol 2μmol/L)、S5组(Propofol 5μmol/L)及S10组(Propofol10μmol/L)。除N组外，其余实验组加入相应浓度的丙泊酚，四组均在常氧培养箱培养48 h,采用CCK-8法检测神经胶质母细胞瘤(U343)活力，流式法检测细胞的凋亡，划痕实验检测细胞迁移能力，蛋白免疫印迹法检测凋亡相关蛋白Caspase-3﹑细胞因子VEGF的表达量。结果：结果CCK-8检测显示，S2组、S5组及S10组OD值低于N组，差异有统计学意义(P<0.05)，且随着丙泊酚浓度的升高细胞活力降低，OD值降低。流式检测显示，S2组、S5组及S10组细胞凋亡率和死亡率高于N组，差异有统计学意义(P<0.05)，且随着培养皿中丙泊酚浓度的升高,细胞凋亡(早期凋亡+晚期凋亡)率和死亡率升高；划痕实验显示：S2组、S5组及S10组迁移率低于N组，差异有统计学意义(P<0.05)，且随着培养皿丙泊酚浓度升高，迁移能力降低;蛋白免疫印迹法显示，S2组、S5组及S10组凋亡相关蛋白Caspase-3表达高于N组，VEGF蛋白表达低于N组,差异有统计学意义(P<0.05)。结论：丙泊酚能降低人神经胶质母细胞瘤(U343)的活力，增加细胞凋亡，抑制肿瘤细胞的增殖和迁移，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.