Reviewer's report
Title:Luteolin decreases IGF-II production and down-regulates insulin-like
growth factor-I receptor signaling in HT-29 human colon cancer cells
Version: 1Date:28 July 2011
Reviewer: Jing Fang
Reviewer's report:
Lim et al demonstrated in the manuscript that luteolin dose-dependently
decreased IGF-II secretion and the expression of IGF-IR precursor protein of
colon cancer HT-29 cells. They found that luteolin decreased IGF-I-induced
tyrosine phosphorylation of IGF-IR and association of p85 with IGF-IR. Moreover,
they reported that luteolin decreased IGF-I-stimulated PI3K/AKT and ERK1/2
signaling. The authors concluded that luteolin down-regulated the activation of
PI3K/Akt and ERK1/2 pathway via decreasing IGF-IR signaling in HT-29 cells,
which may be one of the mechanisms responsible for the luteolin-induced
apoptosis and cell cycle arrest. Generally, the study is quite primarily. It has been
reported that luteolin inhibited IGF-1/IGF-1R signaling and its downstream
targets AKT and ERK (Carcinogenesis vol.28 no.3 pp.713–723, 2007).
Therefore, the novelty of the current work is limited.
Major comments
The authors showed that luteolin inhibited IGF-1/IGF-1R signaling. However, it is
not clear whether or not this inhibition plays a major role in the luteolin-induced
repression of cell proliferation and cell apoptosis.
1. Does the inhibition of IGF/IGF-1R signaling lead to suppression of proliferation
or apoptosis of HT29? Does neutralization of IGF-II results in repression of
proliferation of HT29 cells?
2. Does luteolin inhibit IGF-1/IGF-1R signaling in other colon cancer cells, such
as HCT116 or SW480?
3. The authors determined the effects of luteolin on expression of IGF-II of HT29
cells (Fig. 1). The cells were incubated in serum-free medium for 24 h, followed
by a treatment of luteolin for another 24 h. It is not clear why the cells were
incubated in serum-free medium. What was the status of the cells after luteolin
treatment under the experimental condition? Was the downregulation of
expression of IGF-II due to inhibition of cell proliferation or due to cell apoptosis?
Minor:
1. The inhibition of IGF-1R mRNA level is minor (Fig. 3B). It is suggested to
perform Real-time PCR to determine the IGF-1R mRNA levels.
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Reviewer's report
Title:Luteolin decreases IGF-II production and down-regulates insulin-like
growth factor-I receptor signaling in HT-29 human colon cancer cells
Version: 1Date:28 July 2011
Reviewer: Jing Fang
Reviewer's report:
Lim et al demonstrated in the manuscript that luteolin dose-dependently
decreased IGF-II secretion and the expression of IGF-IR precursor protein of
colon cancer HT-29 cells. They found that luteolin decreased IGF-I-induced
tyrosine phosphorylation of IGF-IR and association of p85 with IGF-IR. Moreover,
they reported that luteolin decreased IGF-I-stimulated PI3K/AKT and ERK1/2
signaling. The authors concluded that luteolin down-regulated the activation of
PI3K/Akt and ERK1/2 pathway via decreasing IGF-IR signaling in HT-29 cells,
which may be one of the mechanisms responsible for the luteolin-induced
apoptosis and cell cycle arrest. Generally, the study is quite primarily. It has been
reported that luteolin inhibited IGF-1/IGF-1R signaling and its downstream
targets AKT and ERK (Carcinogenesis vol.28 no.3 pp.713–723, 2007).
Therefore, the novelty of the current work is limited.
Major comments
The authors showed that luteolin inhibited IGF-1/IGF-1R signaling. However, it is
not clear whether or not this inhibition plays a major role in the luteolin-induced
repression of cell proliferation and cell apoptosis.
1. Does the inhibition of IGF/IGF-1R signaling lead to suppression of proliferation
or apoptosis of HT29? Does neutralization of IGF-II results in repression of
proliferation of HT29 cells?
2. Does luteolin inhibit IGF-1/IGF-1R signaling in other colon cancer cells, such
as HCT116 or SW480?
3. The authors determined the effects of luteolin on expression of IGF-II of HT29
cells (Fig. 1). The cells were incubated in serum-free medium for 24 h, followed
by a treatment of luteolin for another 24 h. It is not clear why the cells were
incubated in serum-free medium. What was the status of the cells after luteolin
treatment under the experimental condition? Was the downregulation of
expression of IGF-II due to inhibition of cell proliferation or due to cell apoptosis?
Minor:
1. The inhibition of IGF-1R mRNA level is minor (Fig. 3B). It is suggested to
perform Real-time PCR to determine the IGF-1R mRNA levels.
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Please review this paper.
user
Reviewer's report
Title:Luteolin decreases IGF-II production and down-regulates insulin-like
growth factor-I receptor signaling in HT-29 human colon cancer cells
Version: 1Date:28 July 2011
Reviewer: Jing Fang
Reviewer's report:
Lim et al demonstrated in the manuscript that luteolin dose-dependently
decreased IGF-II secretion and the expression of IGF-IR precursor protein of
colon cancer HT-29 cells. They found that luteolin decreased IGF-I-induced
tyrosine phosphorylation of IGF-IR and association of p85 with IGF-IR. Moreover,
they reported that luteolin decreased IGF-I-stimulated PI3K/AKT and ERK1/2
signaling. The authors concluded that luteolin down-regulated the activation of
PI3K/Akt and ERK1/2 pathway via decreasing IGF-IR signaling in HT-29 cells,
which may be one of the mechanisms responsible for the luteolin-induced
apoptosis and cell cycle arrest. Generally, the study is quite primarily. It has been
reported that luteolin inhibited IGF-1/IGF-1R signaling and its downstream
targets AKT and ERK (Carcinogenesis vol.28 no.3 pp.713–723, 2007).
Therefore, the novelty of the current work is limited.
Major comments
The authors showed that luteolin inhibited IGF-1/IGF-1R signaling. However, it is
not clear whether or not this inhibition plays a major role in the luteolin-induced
repression of cell proliferation and cell apoptosis.
1. Does the inhibition of IGF/IGF-1R signaling lead to suppression of proliferation
or apoptosis of HT29? Does neutralization of IGF-II results in repression of
proliferation of HT29 cells?
2. Does luteolin inhibit IGF-1/IGF-1R signaling in other colon cancer cells, such
as HCT116 or SW480?
3. The authors determined the effects of luteolin on expression of IGF-II of HT29
cells (Fig. 1). The cells were incubated in serum-free medium for 24 h, followed
by a treatment of luteolin for another 24 h. It is not clear why the cells were
incubated in serum-free medium. What was the status of the cells after luteolin
treatment under the experimental condition? Was the downregulation of
expression of IGF-II due to inhibition of cell proliferation or due to cell apoptosis?
Minor:
1. The inhibition of IGF-1R mRNA level is minor (Fig. 3B). It is suggested to
perform Real-time PCR to determine the IGF-1R mRNA levels.
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
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