j********r
发帖数: 156 | 1 最近观察到一个现象，百思不解，各位帮忙分析一下。
某癌细胞中, 稳转 tet-on shRNA vector targeting gene x (which is a
potential oncogene). 加Dox 3-4天，发现细胞明显停止生长，死细胞增多 (also
there
is induction of PARP cleavage). Akt phosphorylation does not change.
However, these seems obviously increased phosphorylation on ERK1/2 and
ribosomal protein S6. Can't figure how cell death occurs in the
presence of mTORC1 (hyper-) activation.大家说说有哪些可能的survival
pathways, 多谢！ |
f*****i
发帖数: 10 | 2 查查oncogene-induced cell death. |
r***e
发帖数: 2539 | 3 oncogene addiction?
一些癌细胞依赖某个oncogene，去掉后不能生长，比如Ras, myc。
【在 j********r 的大作中提到】
: 最近观察到一个现象，百思不解，各位帮忙分析一下。
: 某癌细胞中, 稳转 tet-on shRNA vector targeting gene x (which is a
: potential oncogene). 加Dox 3-4天，发现细胞明显停止生长，死细胞增多 (also
: there
: is induction of PARP cleavage). Akt phosphorylation does not change.
: However, these seems obviously increased phosphorylation on ERK1/2 and
: ribosomal protein S6. Can't figure how cell death occurs in the
: presence of mTORC1 (hyper-) activation.大家说说有哪些可能的survival
: pathways, 多谢！
|
l**********n
发帖数: 240 | 4 how about your cells with control-shRNA?
I suppose you have one as control.
【在 j********r 的大作中提到】
: 最近观察到一个现象，百思不解，各位帮忙分析一下。
: 某癌细胞中, 稳转 tet-on shRNA vector targeting gene x (which is a
: potential oncogene). 加Dox 3-4天，发现细胞明显停止生长，死细胞增多 (also
: there
: is induction of PARP cleavage). Akt phosphorylation does not change.
: However, these seems obviously increased phosphorylation on ERK1/2 and
: ribosomal protein S6. Can't figure how cell death occurs in the
: presence of mTORC1 (hyper-) activation.大家说说有哪些可能的survival
: pathways, 多谢！
|
h******y
发帖数: 1374 | 5 没有加Dox的就是control呀
【在 l**********n 的大作中提到】
: how about your cells with control-shRNA?
: I suppose you have one as control.
|
j********r
发帖数: 156 | 6 Thanks for the replies. I do have the scramble control, and there is no
difference between minus dox and plus dox. Also another shRNA (which does
not knockdown the target gene expression pretty much based on rt and western
data) doesn't show dox-induced cell death.
This gene product seems highly transforming. I am wondering how cell death
occurs in the presence of increased phosphorylation of those growth/
transformation-correlated factors, like s6 and Erk. (though it is possible
they might co-exist in the pool but not the same cells). |
j********r
发帖数: 156 | 7 another thing which I did not mention is that gene knocking down-induced
cell death became less in the absence of serum.
In comparison, some oncogenes or oncogenic mutations often do not offer
growth advantage in nutrients-abundant conditions. |
