Title: Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis
in colorectal cancer
Version: 3 Date: 13 Jan 2025
Reviewer:  Mohamed H. Zidan
Reviewer's report:
Dear Authors,
Re: The manuscript titled "Amarogentin Suppresses Cell Proliferation and EMT Process
Through Inducing Ferroptosis in Colorectal Cancer"
The study's statistical methods and data analysis, particularly for IC50 determination and
significance testing (Figures 1A and 5A), are appropriately conducted, though some biological
interpretations (e.g., clinical implications of IC50 values) lack depth. The manuscript addresses
this gap by emphasizing IC50's importance in drug efficacy but could further compare AG's
potency with established CRC therapeutics.
While the results strongly indicate pathway modulation, the mechanistic insights remain
speculative. For example, the study does not elucidate whether AG directly affects
transcriptional activity or post-translational stability of these proteins. This limitation,
acknowledged by the authors, is a critical area for future exploration.
The use of patient-derived tumor-like cell clusters (PTCs) enhances the translational relevance
of findings. However, as noted by reviewers, the study does not sufficiently discuss the
heterogeneity of CRC tumors and how well PTCs mimic the tumor microenvironment,
particularly interactions with immune and stromal cells. This oversight limits the broader
applicability of the findings to clinical settings.
The in vivo experiments effectively demonstrate AG's tumor-suppressive effects, supported
by reductions in tumor volume and weight. However, the description of dosing regimens
and therapeutic efficacy, while improved in the revision, remains succinct. Greater detail in
presenting tumor growth inhibition percentages and statistical analyses would enhance the rigor
of this section.
The manuscript's writing quality, while improved, still suffers from occasional lapses in
scientific tone and grammatical clarity (e.g., "AG has been verified to own ameliorative
properties"). These issues, highlighted by reviewers, appear to have been addressed partially but
require additional polishing for academic rigor.
Kind regards
Title: Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis
in colorectal cancer
Version: 3 Date: 13 Jan 2025
Reviewer:  Mohamed H. Zidan
Reviewer's report:
Dear Authors,
Re: The manuscript titled "Amarogentin Suppresses Cell Proliferation and EMT Process
Through Inducing Ferroptosis in Colorectal Cancer"
The study's statistical methods and data analysis, particularly for IC50 determination and
significance testing (Figures 1A and 5A), are appropriately conducted, though some biological
interpretations (e.g., clinical implications of IC50 values) lack depth. The manuscript addresses
this gap by emphasizing IC50's importance in drug efficacy but could further compare AG's
potency with established CRC therapeutics.
While the results strongly indicate pathway modulation, the mechanistic insights remain
speculative. For example, the study does not elucidate whether AG directly affects
transcriptional activity or post-translational stability of these proteins. This limitation,
acknowledged by the authors, is a critical area for future exploration.
The use of patient-derived tumor-like cell clusters (PTCs) enhances the translational relevance
of findings. However, as noted by reviewers, the study does not sufficiently discuss the
heterogeneity of CRC tumors and how well PTCs mimic the tumor microenvironment,
particularly interactions with immune and stromal cells. This oversight limits the broader
applicability of the findings to clinical settings.
The in vivo experiments effectively demonstrate AG's tumor-suppressive effects, supported
by reductions in tumor volume and weight. However, the description of dosing regimens
and therapeutic efficacy, while improved in the revision, remains succinct. Greater detail in
presenting tumor growth inhibition percentages and statistical analyses would enhance the rigor
of this section.
The manuscript's writing quality, while improved, still suffers from occasional lapses in
scientific tone and grammatical clarity (e.g., "AG has been verified to own ameliorative
properties"). These issues, highlighted by reviewers, appear to have been addressed partially but
require additional polishing for academic rigor.
Kind regards
Please review this paper.
user
Title: Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis
in colorectal cancer
Version: 3 Date: 13 Jan 2025
Reviewer:  Mohamed H. Zidan
Reviewer's report:
Dear Authors,
Re: The manuscript titled "Amarogentin Suppresses Cell Proliferation and EMT Process
Through Inducing Ferroptosis in Colorectal Cancer"
The study's statistical methods and data analysis, particularly for IC50 determination and
significance testing (Figures 1A and 5A), are appropriately conducted, though some biological
interpretations (e.g., clinical implications of IC50 values) lack depth. The manuscript addresses
this gap by emphasizing IC50's importance in drug efficacy but could further compare AG's
potency with established CRC therapeutics.
While the results strongly indicate pathway modulation, the mechanistic insights remain
speculative. For example, the study does not elucidate whether AG directly affects
transcriptional activity or post-translational stability of these proteins. This limitation,
acknowledged by the authors, is a critical area for future exploration.
The use of patient-derived tumor-like cell clusters (PTCs) enhances the translational relevance
of findings. However, as noted by reviewers, the study does not sufficiently discuss the
heterogeneity of CRC tumors and how well PTCs mimic the tumor microenvironment,
particularly interactions with immune and stromal cells. This oversight limits the broader
applicability of the findings to clinical settings.
The in vivo experiments effectively demonstrate AG's tumor-suppressive effects, supported
by reductions in tumor volume and weight. However, the description of dosing regimens
and therapeutic efficacy, while improved in the revision, remains succinct. Greater detail in
presenting tumor growth inhibition percentages and statistical analyses would enhance the rigor
of this section.
The manuscript's writing quality, while improved, still suffers from occasional lapses in
scientific tone and grammatical clarity (e.g., "AG has been verified to own ameliorative
properties"). These issues, highlighted by reviewers, appear to have been addressed partially but
require additional polishing for academic rigor.
Kind regards
assistant