Development and validation of a lipogenic genes panel for diagnosis and recurrence of colorectal cancer

Figures

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  Fig 1. Receiver operating characteristics (ROC) curve analysis of the log it model with the ACOT8/ACSL5/FASN/HMGBCS2/SCD1 panel in the training set. The study group consisted of 257 CRC tumor specimens and matched adjacent normal tissues. Using the optimal cutoff value as 0.493, the diagnostic performance of gene panel for discriminating (A) All TNM stages, (B) early CRC (I-II TNM stages), and (C) advanced CRC (III-IV TNM stages) from healthy samples was examined. Log it (p) of model was 0.429 + 0.659 x ACOT8 + 0.084 x ACSL5 + 0.029 x FASN + 0.201 x HMGCS2 + 0.119 x SCD1.

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  Fig 2. Receiver operating characteristics (ROC) curve analysis of the log it model with the ACOT8/ACSL5/FASN/HMGBCS2/SCD1 panel in the validation set I. The study group consisted of 223 CRC tumor specimens and matched adjacent normal tissues. Using the optimal cutoff value as 0.493, the diagnostic performance of gene panel for discriminating (A) All TNM stages, (B) early CRC (I-II TNM stages), and (C) advanced CRC (III-IV TNM stages) from healthy samples was examined. Log it (p) of model was 0.429 + 0.659 x ACOT8 + 0.084 x ACSL5 + 0.029 x FASN + 0.201 x HMGCS2 + 0.119 x SCD1.

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  Fig 3. Receiver operating characteristics (ROC) curve analysis of the log it model with the ACOT8/ACSL5/FASN/HMGBCS2/SCD1 panel in validation set II. The study group consisted of 203 CRC tumor specimens and 50 normal tissues. Using the optimal cutoff value as 0.493, the diagnostic performance of gene panel for discriminating (A) All TNM stages, (B) early CRC (I-II TNM stages, n = 113), and (C) advanced CRC (III-IV TNM stages, n = 90) from healthy samples was examined. Log it (p) of model was 0.429 + 0.659 x ACOT8 + 0.084 x ACSL5 + 0.029 x FASN + 0.201 x HMGCS2 + 0.119 x SCD1.

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  Fig 4. Correlation between the abnormal expression of ACOT8, ACSL5, FASN, HMGCS2, and SCD1 genes and overall survival (OS) of colon cancer patients. (A-E) Training group, (F-J) Validation I group, and (L-O) Validation II group. Kaplan-Meier analysis indicated a reverse correlation between individual genes upregulation and poor survival of CRC patients. (Training group n = 257, Validation group I n = 223, Validation group II n = 203.

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  Fig 5. Correlation between the expression of lipogenic genes panel and overall survival (OS) of colon cancer patients. (A) Training group, (B) Validation group I, and (C) validation group II. OS analysis of lipogenic genes panel showed a statistical correlation between the high predicted point of genes panel and worse OS of CRC patients. (Training group (n = 257): Low risk n = 54, High risk n = 202; Validation group I (n = 223): Low risk n = 52, High risk n = 171; Validation group II (n = 203): Low risk n = 63, High risk n = 140).

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  Fig 6. Schematic view of the roles of ACOT8, ACSL5, FASN, HMGBCS2, and SCD1 genes in lipid metabolism.