Review for 10.1186/s12876-023-02850-z (2023)

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
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paper?
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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
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