Objective To investigate the effect of xenoestrogen nonylphenol (NP) on the proliferation, invasion, and migration of colorectal cancer cells and its relationship with sulfiredoxin-1 ( SRXN1 ) expression. Methods Transcriptomic sequencing and qRT-PCR were used to analyze the effect of NP, SRXN1 expression in colorectal cancer cells. SRXN1 expression in colorectal cancer was analyzed by TCGA and immunohistochemistry. After SRXN1 knockdown in colorectal cancer cell line COLO205 by a specific small interfering RNA ( si-SRXN1 ), effects on the activity, proliferation, ROS release, invasion, and migration of NP (10^-6 mol / L)-treated COLO205 cells was detected by CCK-8, colony formation, transwell, and invasion assays. ERK1 / 2, PI3K/ Akt and Wnt / β-catenin expression was assessed by Western blot. Results Transcriptome sequencing and qRT-PCR analysis showed that NP significantly upregulated SRXN1 expression in COLO205 cells. TCGA and IHC analysis showed that SRXN1 expression in colorectal cancer tissue samples was significantly higher than that in the paracancerous group (P<0. 01). Compared with control group, NP significantly promoted COLO205 cell viability, colony formation, invasion, and migration (P<0. 01). si-SRXN1 significantly inhibited cell proliferation, invasion, and migration (P< 0. 01). Compared with the si-SRXN1 group, cell viability ( P< 0. 01), colony formation (P<0. 05), invasion (P<0. 01), and migration (P<0. 01) were significantly increased in the NP+si- SRXN1 group. Western blotting showed that, compared with the control group, ERK1 / 2, PI3K/ Akt, and Wnt / β-catenin were significantly increased in the NP group ( all P<0. 01) and significantly decreased in the si-SRXN1 group ( all P< 0. 01). Compared with the si-SRXN1 group, ERK1 / 2, PI3K/ Akt and Wnt / β-catenin were significantly increased the in NP+si-SRXN1 group (P<0. 05 or P<0. 01). Conclusions NP promotes the proliferation, invasion, and metastasis of colorectal cancer cells by promoting SRXN1 expression.