科普课堂 | 人结直肠腺癌细胞:COLO320HSR
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科普课堂 | 人结直肠腺癌细胞:COLO320HSR

1.细胞的基础信息

   

名称

人结直肠腺癌细胞:COLO320HSR(STR鉴定正确)

别称

COLO320HSRCOLO-320HSRCOLO-320-HSR; COLO 320 (HSR

种属

生长特性

贴壁生长

细胞形态

成团,圆形的并能折光的

生长培养基

90%RPMI-1640+10%FBS

冻存条件

冻存液:90%FBS+10%DMSO

温度:液氮

培养条件

气相:空气,95%;CO2,5%

温度:37℃

推荐传代比例

1:2~1:3

推荐换液频率

2~3/

 

注意事项

 

 

该细胞为半悬浮和半贴壁细胞 ,悬浮细胞离心收集 ,贴壁细胞消化处理

2.细胞常见的研究有哪些?

a)研究结直肠腺癌的生物学特性

b)药物筛选癌症治疗的研发

c)构建结直肠癌类器官模型

d)有关结直肠腺癌分子发病机制研究

 

3.细胞相关的文献有哪些?

(1)周晓华,黄亮,田由京等.LncRNA PCAT1对结直肠癌Colo320细胞的影响及作用机制研究[J].中国现代普通外科进展,2022,25(08):600-607.

(目的:探讨长链非编码RNALncRNA前列腺癌相关转录本1PCAT1Colo320细胞增殖、侵袭和化疗敏感性的影响及其作用机制。方法:实时荧光定量PCR检测LncRNA PCAT1miR-145-5p和肌动蛋白结合蛋白1FSCN1在结直肠癌组织、Colo3205-Fu耐药细胞株中的表达;分析LncRNA PCAT1miR-145-5pmiR-145-5pFSCN1之间的作用靶点。检测下调PCAT1miR-145-5pFSCN1Colo320细胞增殖和侵袭的影响;检测5-Fu耐药细胞株细胞活力和凋亡率的变化;检测上调LncRNA PCAT1Colo320细胞增殖、侵袭和化疗敏感性的影响。结果:结直肠癌组织和Colo320细胞中LncRNA PCAT1

FSCN1表达上调,miR-145-5p表达下调;5-Fu耐药细胞株中LncRNA PCAT1FSCN1表达下调,miR-145-5p表达上调。LncRNA PCAT1靶向miR-145-5p;miR-145-5p靶向FSCN1。上调LncRNA PCAT1通过miR-145-5p促进Colo320细胞增殖和侵袭。结论:LncRNA PCAT1通过miR-145-5p/FSCN1轴调控Colo320细胞增殖、侵袭及其化疗敏感性。)

 

2)Hori H, Nakata H, Iguchi G, Yamada H, Chihara K, Baba H. Oncogenic ras induces gastrin/CCKB receptor gene expression in human colon cancer cell lines LoVo and Colo320HSR. J Lab Clin Med. 2003 May;141(5):335-41. doi: 10.1016/S0022-2143(03)00021-0. PMID: 12761477.

Gastrin has the ability to stimulate cell growth in some colorectal cancer cells and some of these cells also express gastrin/CCKB receptors, suggesting that gastrin and its autocrine loop are involved in their proliferation. We previously reported that oncogenic ras induced gastrin gene expression in colon cancer cells. The aim of this study was to investigate whether oncogenic ras also induces gastrin/CCKB receptor gene expression. A transiently transfected activated ras vector stimulated gastrin/CCKB receptor transcriptional activities in both Colo320HSR and LoVo cells, but these ras-increased activities were inhibited by a specific MEK inhibitor, PD98059. An RPA demonstrated that activated ras increased endogenous gastrin/CCKB receptor mRNA levels and PD98059 decreased them in LoVo cells. These findings suggest that oncogenic ras induces gastrin/CCKB receptor gene expression through some intracellular signaling pathways, including MEK, in colon cancer cell lines.

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