Reviewer’s report
Title: 
SMC1A facilitates gastric cancer cell proliferation, migration and invasion
via promoting SNAIL activated EMT
Version: 
1 
Date: 
17 Feb 2023
Reviewer's report:
PEER REVIEWER ASSESSMENTS: 
OBJECTIVE - Full research articles: is there a clear objective that addresses a
testable research question(s) (brief or other article types: is there a clear
objective)?
Yes - there is a clear objective
DESIGN - Is the current approach (including controls and analysis protocols)
appropriate for the objective?
No - there are minor issues
EXECUTION - Are the experiments and analyses performed with technical rigor
to allow confidence in the results?
Yes - experiments and analyses were performed appropriately
STATISTICS - Is the use of statistics in the manuscript appropriate?
Not sure - I am not able to assess the statistics in this study
INTERPRETATION - Is the current interpretation/discussion of the results
reasonable and not overstated?
No - there are minor issues
OVERALL MANUSCRIPT POTENTIAL - Is the current version of this work
technically sound? If not, can revisions be made to make the work technically
sound?
Probably - with minor revisions
PEER REVIEWER COMMENTS: 
GENERAL COMMENTS: SMC1A is implicated in tumorigenesis. The authors
report the
underlying mechanisms of SMC1A in gastric cancer (GC).
They used RT-qPCR and western blot to examine the
expression levels of SMC1A in GC tissues and cell lines. The functional role of
SMC1A in cell proliferation, migration, invasion, and the epithelial-
mesenchymal transition. They found that SMC1A was upregulated in GC tissues
and cell lines and correlated with survival in patients. The overexpression of
SMC1A in cells increased 
proliferation, migration, and invasion, and the
knockdown of SMC1A in HCG27 
cells inhibited cell proliferation, migration,
and invasion of HGC27 cells. The authors report a series of in vitro functional
studies supporting SMC1A in GC pathogenesis.
The methods section was presented in detail. Functionally, they claim that
SMC1A promoted EMT via upregulating SNAIL.
Table 1 should be shown as supplementary data. The authors should show the
protein expression in GC tumor tissues from patients. Without this data, it is
unclear if there is functional relevance of SMC1A in tumor tissues. Further, they
have generated the SMC1A cells with overexpression and knockout. If they have
stable expression, these cells should be evaluated in straightforward Skid/nude
mouse models with subcutaneous tumors. Currently, the conclusions are based
on in vitro data, which lack in vivo validation.
REQUESTED REVISIONS: 
This study by the authors sheds light on the role of SMC1A in gastric cancer
(GC) and the underlying mechanisms behind it. The authors utilized various
techniques such as RT-qPCR and western blot to examine the expression levels
of SMC1A in GC tissues and cell lines. Their findings showed that SMC1A was
upregulated in GC tissues and cell lines and correlated with patient survival.
The authors also conducted in vitro functional studies to examine the role of
SMC1A in cell proliferation, migration, invasion, and epithelial-mesenchymal
transition. They reported that the overexpression of SMC1A in cells increased
proliferation, migration, and invasion, and the knockdown of SMC1A inhibited
these processes in HGC27 cells.
Although the methods section was presented in detail, there are some concerns
regarding the study. Table 1 should be shown as supplementary data, and the
authors should show the protein expression in GC tumor tissues from patients.
This data is crucial in establishing the functional relevance of SMC1A in tumor
tissues.
Additionally, the authors have generated SMC1A cells with overexpression and
knockout, and if they have stable expression, these cells should be evaluated in
straightforward Skid/nude mouse models with subcutaneous tumors. Currently,
the conclusions are based solely on in vitro data, which lack in vivo validation.
Overall, the study provides valuable insights into the role of SMC1A in GC
pathogenesis, but further research is required to validate the in vitro findings in
an in vivo setting.
Declaration of competing interests
Please complete a declaration of competing
interests, considering the following questions:
1
. 
Have you in the past five years received reimbursements, fees, funding, or
salary from an organisation that may in any way gain or lose financially
from the publication of this manuscript, either now or in the future?
2
. 
Do you hold any stocks or shares in an organisation that may in any way
gain or lose financially from the publication of this manuscript, either now
or in the future?
3
. 
Do you hold or are you currently applying for any patents relating to the
content of the manuscript?
4
. 
Have you received reimbursements, fees, funding, or salary from an
organization that holds or has applied for patents relating to the content of
the manuscript?
5
. 
Do you have any other financial competing interests?
6
. 
Do you have any non-financial competing interests in relation to this
paper?
If you can answer no to all of the above, write 'I declare that I have no competing
interests' below. If your reply is yes to any, please give details below.
This reviewer has been recruited by a partner organization, Research Square.
Reviewers with declared or apparent competing interests are not utilized for
these reviews. This reviewer has agreed to publication of their comments online
under a Creative Commons Attribution License attributed to Research Square
and was paid a small honorarium for completing the review within a specified
timeframe. Honoraria for reviews such as this are paid regardless of the reviewer
recommendation.
Reviewer Publication Consent.
 I agree for my report to be made available
under an Open Access Creative Commons CC-BY License (
http://creativecommons.org/licenses/by/4.0
) if this manuscript is accepted for
publication. Any comments that I do not wish to be included in the published
report have been included as confidential comments to the editor, which will not
be published.
If you are not happy for us to publish this report, please contact the
editorial office before completing the review.
If you wish, you can include your
name in your published report. Please note you must decide whether to include
your name at the start of the process and confirm this decision whenever
prompted. If you change your decision later, we will not be able to publish your
name.
I agree to the terms of the CC-BY 4.0 license; please 
do not
 publish my name
with my report. (default)
Is the study design appropriate to answer the research question (including the use
of appropriate controls), and are the conclusions supported by the evidence
presented?
No
Are the methods sufficiently described to allow the study to be repeated?
No
Is the use of statistics and treatment of uncertainties appropriate?
Yes
Is the presentation of the work clear?
No
Are the images in this manuscript (including electrophoretic gels and blots) free
from apparent manipulation?
Yes
Web of Science Reviewer Recognition
. Springer Nature can send verification
of this review directly to a Web of Science researcher profile (a subsidiary of
Clarivate Analytics). If you would like to take advantage of this service, please
click on the “Yes” option below. Your name, email address, title of the reviewed
manuscript, name of the journal, and date of your review submission (the
“Review Data”) will then be transmitted to Web of Science after the final
decision on the manuscript has been made. If you have already registered with
Web of Science for a 
Web of Science researcher profile (this service was
previously known as “Publons”), they will notify you of the receipt of this
review and update your profile as per your settings and their policy. If you are
not registered with Web of Science, you will receive an email from them asking
you to register in order for them to be able to recognize your review on your new
profile page. Web of Science may use the Review Data to generate derivative
metadata for the benefit of Web of Science and you as a reviewer, carefully
considering the sensitivity of such information. For example, Web of Science
may verify your record as a reviewer by updating your profile published on its
webservice if you have registered for such service or help editors to identify
candidate reviewers. Please find the details of processing in Web of Science’s
privacy policy 
https://clarivate.com/privacy-center/notices-policies/privacy-
policy/
No
Reviewer’s report
Title: 
SMC1A facilitates gastric cancer cell proliferation, migration and invasion
via promoting SNAIL activated EMT
Version: 
1 
Date: 
17 Feb 2023
Reviewer's report:
PEER REVIEWER ASSESSMENTS: 
OBJECTIVE - Full research articles: is there a clear objective that addresses a
testable research question(s) (brief or other article types: is there a clear
objective)?
Yes - there is a clear objective
DESIGN - Is the current approach (including controls and analysis protocols)
appropriate for the objective?
No - there are minor issues
EXECUTION - Are the experiments and analyses performed with technical rigor
to allow confidence in the results?
Yes - experiments and analyses were performed appropriately
STATISTICS - Is the use of statistics in the manuscript appropriate?
Not sure - I am not able to assess the statistics in this study
INTERPRETATION - Is the current interpretation/discussion of the results
reasonable and not overstated?
No - there are minor issues
OVERALL MANUSCRIPT POTENTIAL - Is the current version of this work
technically sound? If not, can revisions be made to make the work technically
sound?
Probably - with minor revisions
PEER REVIEWER COMMENTS: 
GENERAL COMMENTS: SMC1A is implicated in tumorigenesis. The authors
report the
underlying mechanisms of SMC1A in gastric cancer (GC).
They used RT-qPCR and western blot to examine the
expression levels of SMC1A in GC tissues and cell lines. The functional role of
SMC1A in cell proliferation, migration, invasion, and the epithelial-
mesenchymal transition. They found that SMC1A was upregulated in GC tissues
and cell lines and correlated with survival in patients. The overexpression of
SMC1A in cells increased 
proliferation, migration, and invasion, and the
knockdown of SMC1A in HCG27 
cells inhibited cell proliferation, migration,
and invasion of HGC27 cells. The authors report a series of in vitro functional
studies supporting SMC1A in GC pathogenesis.
The methods section was presented in detail. Functionally, they claim that
SMC1A promoted EMT via upregulating SNAIL.
Table 1 should be shown as supplementary data. The authors should show the
protein expression in GC tumor tissues from patients. Without this data, it is
unclear if there is functional relevance of SMC1A in tumor tissues. Further, they
have generated the SMC1A cells with overexpression and knockout. If they have
stable expression, these cells should be evaluated in straightforward Skid/nude
mouse models with subcutaneous tumors. Currently, the conclusions are based
on in vitro data, which lack in vivo validation.
REQUESTED REVISIONS: 
This study by the authors sheds light on the role of SMC1A in gastric cancer
(GC) and the underlying mechanisms behind it. The authors utilized various
techniques such as RT-qPCR and western blot to examine the expression levels
of SMC1A in GC tissues and cell lines. Their findings showed that SMC1A was
upregulated in GC tissues and cell lines and correlated with patient survival.
The authors also conducted in vitro functional studies to examine the role of
SMC1A in cell proliferation, migration, invasion, and epithelial-mesenchymal
transition. They reported that the overexpression of SMC1A in cells increased
proliferation, migration, and invasion, and the knockdown of SMC1A inhibited
these processes in HGC27 cells.
Although the methods section was presented in detail, there are some concerns
regarding the study. Table 1 should be shown as supplementary data, and the
authors should show the protein expression in GC tumor tissues from patients.
This data is crucial in establishing the functional relevance of SMC1A in tumor
tissues.
Additionally, the authors have generated SMC1A cells with overexpression and
knockout, and if they have stable expression, these cells should be evaluated in
straightforward Skid/nude mouse models with subcutaneous tumors. Currently,
the conclusions are based solely on in vitro data, which lack in vivo validation.
Overall, the study provides valuable insights into the role of SMC1A in GC
pathogenesis, but further research is required to validate the in vitro findings in
an in vivo setting.
Declaration of competing interests
Please complete a declaration of competing
interests, considering the following questions:
1
. 
Have you in the past five years received reimbursements, fees, funding, or
salary from an organisation that may in any way gain or lose financially
from the publication of this manuscript, either now or in the future?
2
. 
Do you hold any stocks or shares in an organisation that may in any way
gain or lose financially from the publication of this manuscript, either now
or in the future?
3
. 
Do you hold or are you currently applying for any patents relating to the
content of the manuscript?
4
. 
Have you received reimbursements, fees, funding, or salary from an
organization that holds or has applied for patents relating to the content of
the manuscript?
5
. 
Do you have any other financial competing interests?
6
. 
Do you have any non-financial competing interests in relation to this
paper?
If you can answer no to all of the above, write 'I declare that I have no competing
interests' below. If your reply is yes to any, please give details below.
This reviewer has been recruited by a partner organization, Research Square.
Reviewers with declared or apparent competing interests are not utilized for
these reviews. This reviewer has agreed to publication of their comments online
under a Creative Commons Attribution License attributed to Research Square
and was paid a small honorarium for completing the review within a specified
timeframe. Honoraria for reviews such as this are paid regardless of the reviewer
recommendation.
Reviewer Publication Consent.
 I agree for my report to be made available
under an Open Access Creative Commons CC-BY License (
http://creativecommons.org/licenses/by/4.0
) if this manuscript is accepted for
publication. Any comments that I do not wish to be included in the published
report have been included as confidential comments to the editor, which will not
be published.
If you are not happy for us to publish this report, please contact the
editorial office before completing the review.
If you wish, you can include your
name in your published report. Please note you must decide whether to include
your name at the start of the process and confirm this decision whenever
prompted. If you change your decision later, we will not be able to publish your
name.
I agree to the terms of the CC-BY 4.0 license; please 
do not
 publish my name
with my report. (default)
Is the study design appropriate to answer the research question (including the use
of appropriate controls), and are the conclusions supported by the evidence
presented?
No
Are the methods sufficiently described to allow the study to be repeated?
No
Is the use of statistics and treatment of uncertainties appropriate?
Yes
Is the presentation of the work clear?
No
Are the images in this manuscript (including electrophoretic gels and blots) free
from apparent manipulation?
Yes
Web of Science Reviewer Recognition
. Springer Nature can send verification
of this review directly to a Web of Science researcher profile (a subsidiary of
Clarivate Analytics). If you would like to take advantage of this service, please
click on the “Yes” option below. Your name, email address, title of the reviewed
manuscript, name of the journal, and date of your review submission (the
“Review Data”) will then be transmitted to Web of Science after the final
decision on the manuscript has been made. If you have already registered with
Web of Science for a 
Web of Science researcher profile (this service was
previously known as “Publons”), they will notify you of the receipt of this
review and update your profile as per your settings and their policy. If you are
not registered with Web of Science, you will receive an email from them asking
you to register in order for them to be able to recognize your review on your new
profile page. Web of Science may use the Review Data to generate derivative
metadata for the benefit of Web of Science and you as a reviewer, carefully
considering the sensitivity of such information. For example, Web of Science
may verify your record as a reviewer by updating your profile published on its
webservice if you have registered for such service or help editors to identify
candidate reviewers. Please find the details of processing in Web of Science’s
privacy policy 
https://clarivate.com/privacy-center/notices-policies/privacy-
policy/
No
Please review this paper.
user
Reviewer’s report
Title: 
SMC1A facilitates gastric cancer cell proliferation, migration and invasion
via promoting SNAIL activated EMT
Version: 
1 
Date: 
17 Feb 2023
Reviewer's report:
PEER REVIEWER ASSESSMENTS: 
OBJECTIVE - Full research articles: is there a clear objective that addresses a
testable research question(s) (brief or other article types: is there a clear
objective)?
Yes - there is a clear objective
DESIGN - Is the current approach (including controls and analysis protocols)
appropriate for the objective?
No - there are minor issues
EXECUTION - Are the experiments and analyses performed with technical rigor
to allow confidence in the results?
Yes - experiments and analyses were performed appropriately
STATISTICS - Is the use of statistics in the manuscript appropriate?
Not sure - I am not able to assess the statistics in this study
INTERPRETATION - Is the current interpretation/discussion of the results
reasonable and not overstated?
No - there are minor issues
OVERALL MANUSCRIPT POTENTIAL - Is the current version of this work
technically sound? If not, can revisions be made to make the work technically
sound?
Probably - with minor revisions
PEER REVIEWER COMMENTS: 
GENERAL COMMENTS: SMC1A is implicated in tumorigenesis. The authors
report the
underlying mechanisms of SMC1A in gastric cancer (GC).
They used RT-qPCR and western blot to examine the
expression levels of SMC1A in GC tissues and cell lines. The functional role of
SMC1A in cell proliferation, migration, invasion, and the epithelial-
mesenchymal transition. They found that SMC1A was upregulated in GC tissues
and cell lines and correlated with survival in patients. The overexpression of
SMC1A in cells increased 
proliferation, migration, and invasion, and the
knockdown of SMC1A in HCG27 
cells inhibited cell proliferation, migration,
and invasion of HGC27 cells. The authors report a series of in vitro functional
studies supporting SMC1A in GC pathogenesis.
The methods section was presented in detail. Functionally, they claim that
SMC1A promoted EMT via upregulating SNAIL.
Table 1 should be shown as supplementary data. The authors should show the
protein expression in GC tumor tissues from patients. Without this data, it is
unclear if there is functional relevance of SMC1A in tumor tissues. Further, they
have generated the SMC1A cells with overexpression and knockout. If they have
stable expression, these cells should be evaluated in straightforward Skid/nude
mouse models with subcutaneous tumors. Currently, the conclusions are based
on in vitro data, which lack in vivo validation.
REQUESTED REVISIONS: 
This study by the authors sheds light on the role of SMC1A in gastric cancer
(GC) and the underlying mechanisms behind it. The authors utilized various
techniques such as RT-qPCR and western blot to examine the expression levels
of SMC1A in GC tissues and cell lines. Their findings showed that SMC1A was
upregulated in GC tissues and cell lines and correlated with patient survival.
The authors also conducted in vitro functional studies to examine the role of
SMC1A in cell proliferation, migration, invasion, and epithelial-mesenchymal
transition. They reported that the overexpression of SMC1A in cells increased
proliferation, migration, and invasion, and the knockdown of SMC1A inhibited
these processes in HGC27 cells.
Although the methods section was presented in detail, there are some concerns
regarding the study. Table 1 should be shown as supplementary data, and the
authors should show the protein expression in GC tumor tissues from patients.
This data is crucial in establishing the functional relevance of SMC1A in tumor
tissues.
Additionally, the authors have generated SMC1A cells with overexpression and
knockout, and if they have stable expression, these cells should be evaluated in
straightforward Skid/nude mouse models with subcutaneous tumors. Currently,
the conclusions are based solely on in vitro data, which lack in vivo validation.
Overall, the study provides valuable insights into the role of SMC1A in GC
pathogenesis, but further research is required to validate the in vitro findings in
an in vivo setting.
Declaration of competing interests
Please complete a declaration of competing
interests, considering the following questions:
1
. 
Have you in the past five years received reimbursements, fees, funding, or
salary from an organisation that may in any way gain or lose financially
from the publication of this manuscript, either now or in the future?
2
. 
Do you hold any stocks or shares in an organisation that may in any way
gain or lose financially from the publication of this manuscript, either now
or in the future?
3
. 
Do you hold or are you currently applying for any patents relating to the
content of the manuscript?
4
. 
Have you received reimbursements, fees, funding, or salary from an
organization that holds or has applied for patents relating to the content of
the manuscript?
5
. 
Do you have any other financial competing interests?
6
. 
Do you have any non-financial competing interests in relation to this
paper?
If you can answer no to all of the above, write 'I declare that I have no competing
interests' below. If your reply is yes to any, please give details below.
This reviewer has been recruited by a partner organization, Research Square.
Reviewers with declared or apparent competing interests are not utilized for
these reviews. This reviewer has agreed to publication of their comments online
under a Creative Commons Attribution License attributed to Research Square
and was paid a small honorarium for completing the review within a specified
timeframe. Honoraria for reviews such as this are paid regardless of the reviewer
recommendation.
Reviewer Publication Consent.
 I agree for my report to be made available
under an Open Access Creative Commons CC-BY License (
http://creativecommons.org/licenses/by/4.0
) if this manuscript is accepted for
publication. Any comments that I do not wish to be included in the published
report have been included as confidential comments to the editor, which will not
be published.
If you are not happy for us to publish this report, please contact the
editorial office before completing the review.
If you wish, you can include your
name in your published report. Please note you must decide whether to include
your name at the start of the process and confirm this decision whenever
prompted. If you change your decision later, we will not be able to publish your
name.
I agree to the terms of the CC-BY 4.0 license; please 
do not
 publish my name
with my report. (default)
Is the study design appropriate to answer the research question (including the use
of appropriate controls), and are the conclusions supported by the evidence
presented?
No
Are the methods sufficiently described to allow the study to be repeated?
No
Is the use of statistics and treatment of uncertainties appropriate?
Yes
Is the presentation of the work clear?
No
Are the images in this manuscript (including electrophoretic gels and blots) free
from apparent manipulation?
Yes
Web of Science Reviewer Recognition
. Springer Nature can send verification
of this review directly to a Web of Science researcher profile (a subsidiary of
Clarivate Analytics). If you would like to take advantage of this service, please
click on the “Yes” option below. Your name, email address, title of the reviewed
manuscript, name of the journal, and date of your review submission (the
“Review Data”) will then be transmitted to Web of Science after the final
decision on the manuscript has been made. If you have already registered with
Web of Science for a 
Web of Science researcher profile (this service was
previously known as “Publons”), they will notify you of the receipt of this
review and update your profile as per your settings and their policy. If you are
not registered with Web of Science, you will receive an email from them asking
you to register in order for them to be able to recognize your review on your new
profile page. Web of Science may use the Review Data to generate derivative
metadata for the benefit of Web of Science and you as a reviewer, carefully
considering the sensitivity of such information. For example, Web of Science
may verify your record as a reviewer by updating your profile published on its
webservice if you have registered for such service or help editors to identify
candidate reviewers. Please find the details of processing in Web of Science’s
privacy policy 
https://clarivate.com/privacy-center/notices-policies/privacy-
policy/
No
assistant