Title: METTL3 regulates N6-methyladenosine modification of ANGPTL3 mRNA and
potentiates malignant progression of stomach adenocarcinoma
Version: 1 Date: 19 Mar 2023
Reviewer's report:
The manuscript by Zhang et al. describes METTL3 regulates N6-methyladenosin modification
of ANGPTL3 mRNA and potentiates malignant progression of STAD. Although the aim
is interesting, this study is too premature to be published. Several issues below should be
considered to improve the quality of this article.
1. Out of six genes (METTL3, WTAP, YTHDF1, YTHDF2, YTHDF3, and HNRNPA2B1).
the authors selected only METTL3 based on reference. Some reports have well known other
candidates (WTAP, YTHDF family ..) can also mediate m6A modification. The authors need to
clearly demonstrate the reason why you selected METTL3 genes.
2. All membranes of western blots have a poor quality. I recommend to supplement whole
membrane as raw data.
3. Unlike your study, high expression of ANGPTL3 has observed in various cancer tissue,
including OSCC, HCC, and ovarian cancer, and it can promote cancer growth, motility, and
invasion. I understand that lower expression and stability of ANGPTL3 can maintain under the
METTL3-silenced condition. If so, did you check the effects of ANGPTL3 (migration, invasion,
and proliferation..), regardless of METTL3-silencing?
To further exactly address the your finding that METTL3 represses ANGPTL3 and its silencing
rescued METTL3 silencing-impeded proliferation, migration, and invasion of STAD, you need
to check the effects of ANGPTL3 in STAD under the control condition (without METTL3
sliencing).
Title: METTL3 regulates N6-methyladenosine modification of ANGPTL3 mRNA and
potentiates malignant progression of stomach adenocarcinoma
Version: 1 Date: 19 Mar 2023
Reviewer's report:
The manuscript by Zhang et al. describes METTL3 regulates N6-methyladenosin modification
of ANGPTL3 mRNA and potentiates malignant progression of STAD. Although the aim
is interesting, this study is too premature to be published. Several issues below should be
considered to improve the quality of this article.
1. Out of six genes (METTL3, WTAP, YTHDF1, YTHDF2, YTHDF3, and HNRNPA2B1).
the authors selected only METTL3 based on reference. Some reports have well known other
candidates (WTAP, YTHDF family ..) can also mediate m6A modification. The authors need to
clearly demonstrate the reason why you selected METTL3 genes.
2. All membranes of western blots have a poor quality. I recommend to supplement whole
membrane as raw data.
3. Unlike your study, high expression of ANGPTL3 has observed in various cancer tissue,
including OSCC, HCC, and ovarian cancer, and it can promote cancer growth, motility, and
invasion. I understand that lower expression and stability of ANGPTL3 can maintain under the
METTL3-silenced condition. If so, did you check the effects of ANGPTL3 (migration, invasion,
and proliferation..), regardless of METTL3-silencing?
To further exactly address the your finding that METTL3 represses ANGPTL3 and its silencing
rescued METTL3 silencing-impeded proliferation, migration, and invasion of STAD, you need
to check the effects of ANGPTL3 in STAD under the control condition (without METTL3
sliencing).
Please review this paper.
user
Title: METTL3 regulates N6-methyladenosine modification of ANGPTL3 mRNA and
potentiates malignant progression of stomach adenocarcinoma
Version: 1 Date: 19 Mar 2023
Reviewer's report:
The manuscript by Zhang et al. describes METTL3 regulates N6-methyladenosin modification
of ANGPTL3 mRNA and potentiates malignant progression of STAD. Although the aim
is interesting, this study is too premature to be published. Several issues below should be
considered to improve the quality of this article.
1. Out of six genes (METTL3, WTAP, YTHDF1, YTHDF2, YTHDF3, and HNRNPA2B1).
the authors selected only METTL3 based on reference. Some reports have well known other
candidates (WTAP, YTHDF family ..) can also mediate m6A modification. The authors need to
clearly demonstrate the reason why you selected METTL3 genes.
2. All membranes of western blots have a poor quality. I recommend to supplement whole
membrane as raw data.
3. Unlike your study, high expression of ANGPTL3 has observed in various cancer tissue,
including OSCC, HCC, and ovarian cancer, and it can promote cancer growth, motility, and
invasion. I understand that lower expression and stability of ANGPTL3 can maintain under the
METTL3-silenced condition. If so, did you check the effects of ANGPTL3 (migration, invasion,
and proliferation..), regardless of METTL3-silencing?
To further exactly address the your finding that METTL3 represses ANGPTL3 and its silencing
rescued METTL3 silencing-impeded proliferation, migration, and invasion of STAD, you need
to check the effects of ANGPTL3 in STAD under the control condition (without METTL3
sliencing).
assistant