Title: COL10A1 promotes tumorigenesis by modulating CD276 in pancreatic adenocarcinoma
Version: 1 Date: 09 Feb 2023
Reviewer's report:
In this study, the authors described the role of COL10A1 in PDAC tumor
Progression, and identified CD276 as a potential target of COL10A1 to promote PDAC
tumorigenesis. There are several limitations to the study which are outlined below.
1. Importantly, COL10A1 viewed as an oncogene in PDAC of this study is contradicted its
low levels among the bioinformatics analysis of GSE62165. Furthermore, COL10A1 as one of
down-regulated DEGs from GSE62165 data is noncoincident to its high expression from the
GEPIA database, a public database. So based on those data, it is not concluded that COL10A1
promoted PDAC development.
2. In the bioinformatics analysis procedure, it was not defined the fold change range of DEGs,
only claimed that the up-limited value is # 2.0 fold change. Followed by the PPI network of
DEGs, it obtained 10 hub genes including COL10A1, however, authors had no certain proof to
target gene as its consequent exploration in PDAC.
3. In wound healing assays, data is controversial, figure 3D where at a 24-hour point, wound
healing lines of both si-NC cells and si-COL10A1 cells showed no significant difference, but the
chat below has revealed significance. Figure 4C where according to the Spearman-Correlation
of both COL10A1 and CD276 valued, it was not supported the association of them. Based on
the only evidence of knockdown experiment, it is not convinced that COL10A1 and CD27 had
related regulation directly or indirectly, need the more molecular mechanism to provide strong
evidence for the conclusion
4. The manuscript should be edited overall for English grammar and language use. Furthermore,
it existed that figures noted are not very clear and some spellings are mistakes.
Title: COL10A1 promotes tumorigenesis by modulating CD276 in pancreatic adenocarcinoma
Version: 1 Date: 09 Feb 2023
Reviewer's report:
In this study, the authors described the role of COL10A1 in PDAC tumor
Progression, and identified CD276 as a potential target of COL10A1 to promote PDAC
tumorigenesis. There are several limitations to the study which are outlined below.
1. Importantly, COL10A1 viewed as an oncogene in PDAC of this study is contradicted its
low levels among the bioinformatics analysis of GSE62165. Furthermore, COL10A1 as one of
down-regulated DEGs from GSE62165 data is noncoincident to its high expression from the
GEPIA database, a public database. So based on those data, it is not concluded that COL10A1
promoted PDAC development.
2. In the bioinformatics analysis procedure, it was not defined the fold change range of DEGs,
only claimed that the up-limited value is # 2.0 fold change. Followed by the PPI network of
DEGs, it obtained 10 hub genes including COL10A1, however, authors had no certain proof to
target gene as its consequent exploration in PDAC.
3. In wound healing assays, data is controversial, figure 3D where at a 24-hour point, wound
healing lines of both si-NC cells and si-COL10A1 cells showed no significant difference, but the
chat below has revealed significance. Figure 4C where according to the Spearman-Correlation
of both COL10A1 and CD276 valued, it was not supported the association of them. Based on
the only evidence of knockdown experiment, it is not convinced that COL10A1 and CD27 had
related regulation directly or indirectly, need the more molecular mechanism to provide strong
evidence for the conclusion
4. The manuscript should be edited overall for English grammar and language use. Furthermore,
it existed that figures noted are not very clear and some spellings are mistakes.
Please review this paper.
user
Title: COL10A1 promotes tumorigenesis by modulating CD276 in pancreatic adenocarcinoma
Version: 1 Date: 09 Feb 2023
Reviewer's report:
In this study, the authors described the role of COL10A1 in PDAC tumor
Progression, and identified CD276 as a potential target of COL10A1 to promote PDAC
tumorigenesis. There are several limitations to the study which are outlined below.
1. Importantly, COL10A1 viewed as an oncogene in PDAC of this study is contradicted its
low levels among the bioinformatics analysis of GSE62165. Furthermore, COL10A1 as one of
down-regulated DEGs from GSE62165 data is noncoincident to its high expression from the
GEPIA database, a public database. So based on those data, it is not concluded that COL10A1
promoted PDAC development.
2. In the bioinformatics analysis procedure, it was not defined the fold change range of DEGs,
only claimed that the up-limited value is # 2.0 fold change. Followed by the PPI network of
DEGs, it obtained 10 hub genes including COL10A1, however, authors had no certain proof to
target gene as its consequent exploration in PDAC.
3. In wound healing assays, data is controversial, figure 3D where at a 24-hour point, wound
healing lines of both si-NC cells and si-COL10A1 cells showed no significant difference, but the
chat below has revealed significance. Figure 4C where according to the Spearman-Correlation
of both COL10A1 and CD276 valued, it was not supported the association of them. Based on
the only evidence of knockdown experiment, it is not convinced that COL10A1 and CD27 had
related regulation directly or indirectly, need the more molecular mechanism to provide strong
evidence for the conclusion
4. The manuscript should be edited overall for English grammar and language use. Furthermore,
it existed that figures noted are not very clear and some spellings are mistakes.
assistant