 
- 积分
- 504
- 威望
- 504
- 包包
- 2301
|
本帖最后由 细胞海洋 于 2013-1-5 09:38 编辑
/ E4 } a5 n2 M* C' p1 b
/ R4 P+ g0 J# h作者:Beyond 发布于2012-9-22 19:27:23
# ]: ? ]- I4 X' B
q& m' v" h: y2012年9月22日 电 /生物谷BIOON/ --近日,冈山大学Masaharu Seno和他的同事已经证明,正常干细胞在体外接触到人为制造的肿瘤微环境会演变成肿瘤干细胞(CSCs)。
7 q+ F% a3 E" Z, n* p& w$ x% h% s6 ?3 C3 r
肿瘤干细胞是肿瘤中具有自我更新能力并能产生异质性肿瘤细胞的细胞。传统观念认为,肿瘤是由体细胞突变而成,每个肿瘤细胞都可以无限制地生长。但这无法解释肿瘤细胞似乎具有无限的生命力以及并非所有肿瘤细胞都能无限制生长的现象。
5 I$ p2 H- s3 P( Q$ `- n! R2 ]
1 r/ x; C+ u" H; \肿瘤细胞生长、转移和复发的特点与干细胞的基本特性十分相似,因此,肿瘤干细胞(CSCs)已被提议作为解释癌细胞扩散的主要原因。
/ C; R4 M: @0 T4 w! |8 q# s# F4 W# V& ~$ p
* Y5 [* n! [! [" A* T研究人员现在已经证明正常干细胞在体外接触到人为制造的肿瘤微环境后会发展成肿瘤干细胞(CSCs)。这项最新研究是由冈山大学教授Masaharu Seno与中国和美国科学家合作完成。6 a1 j+ I& e2 O z9 ]0 q
" ~- ]( z0 W. W) f, c
研究者从小鼠肿瘤细胞株来源的条件培养基培养小鼠诱导多能干细胞,发现在体内也具有致瘤性。肿瘤干细胞及其产生过程的研究将有助于分析肿瘤微环境的遗传改变和分泌因子对诱导多能干细胞转换为干细胞的确切作用,研究工作也有助于开发对抗癌症的新疗法。* b- ~" h* w d+ o
1 a$ h( [0 k1 g) p) D, |2 z0 D
k. `% N8 @: V, j' g$ m# J/ Q5 v, w+ k5 _
5 Z5 D+ z6 n; S" G. g1 _ M% U' E/ Y" U2 ? T% h( k" _7 C% j0 G% V4 _: B
doi:10.1371/journal.pone.0033544
- K& j* C: I& p0 u' A+ C3 UPMC:# Q! R0 {- v8 h% v& _9 f2 W
PMID:& m" G& `$ O0 D+ H
0 X7 Y, W' T0 D! f$ o" j* VA Model of Cancer Stem Cells Derived from Mouse Induced Pluripotent Stem Cells
' l- Y! ]) E1 ?0 V& C5 x o: \+ u2 S4 t" \% U7 C9 _" K$ H0 {
Ling Chen, Tomonari Kasai, Yueguang Li, Yuh Sugii, Guoliang Jin, Masashi Okada, Arun Vaidyanath, Akifumi Mizutani, Ayano Satoh, Takayuki Kudoh, Mary J. C. Hendrix, David S. Salomon, Li Fu*, Masaharu Seno*9 s7 R3 ?' v5 W
5 i) ]7 x9 g+ L c5 R) Z1 L' n
Cancer stem cells (CSCs) are capable of continuous proliferation and self-renewal and are proposed to play significant roles in oncogenesis, tumor growth, metastasis and cancer recurrence. CSCs are considered derived from normal stem cells affected by the tumor microenvironment although the mechanism of development is not clear yet. In 2007, Yamanaka's group succeeded in generating Nanog mouse induced pluripotent stem (miPS) cells, in which green fluorescent protein (GFP) has been inserted into the 5′-untranslated region of the Nanog gene. Usually, iPS cells, just like embryonic stem cells, are considered to be induced into progenitor cells, which differentiate into various normal phenotypes depending on the normal niche. We hypothesized that CSCs could be derived from Nanog miPS cells in the conditioned culture medium of cancer cell lines, which is a mimic of carcinoma microenvironment. As a result, the Nanog miPS cells treated with the conditioned medium of mouse Lewis lung carcinoma acquired characteristics of CSCs, in that they formed spheroids expressing GFP in suspension culture, and had a high tumorigenicity in Balb/c nude mice exhibiting angiogenesis in vivo. In addition, these iPS-derived CSCs had a capacity of self-renewal and expressed the marker genes, Nanog, Rex1, Eras, Esg1 and Cripto, associated with stem cell properties and an undifferentiated state. Thus we concluded that a model of CSCs was originally developed from miPS cells and proposed the conditioned culture medium of cancer cell lines might perform as niche for producing CSCs. The model of CSCs and the procedure of their establishment will help study the genetic alterations and the secreted factors in the tumor microenvironment which convert miPS cells to CSCs. Furthermore, the identification of potentially bona fide markers of CSCs, which will help the development of novel anti-cancer therapies, might be possible though the CSC model.
# H8 p8 Q$ ]6 x1 ~0 j% J- E, r+ c% u3 x7 w% g
|
|