Related Experiment Video
Updated: May 12, 2026

Comparative Strategies for Ubiquitination Detection in Mammalian Cell Lysates Using SMAD2/SMURF2 as a Model
Published on: April 17, 2026
Reduced expression of SM22 is correlated with low autophagy activity in human colorectal cancer
Xiao-Li Xie1, Ya-Bin Liu, Yue-Ping Liu
1Department of Biochemistry and Molecular Biology, College of Basic Medicine, Key Laboratory of Medical Biotechnology of Hebei Province, Hebei Medical University, Shijiazhuang 050017, PR China.
Abstract:
Colorectal cancer (CRC) is a common malignancy with a high incidence and mortality rate. Recent studies have pointed to deregulation of autophagy as a novel pathogenesis of human malignancy. SM22 is considered as a tumor suppressor. The aim of the present study was to evaluate the correlation of the SM22 expression level with the autophagy activity and the clinical characteristics in human CRC tissues. The expressions of SM22 and p62, a biomarker of autophagy activity, in paired tumor and adjacent non-tumor tissues from 43 patients with colorectal cancer were detected by western blot and immunohistochemical staining, respectively. The results showed that the SM22 level decreased significantly in 81.4% CRC tissues, while the expression of p62 increased in 79.1% cases. There was a negative correlation between p62 and SM22 expressions in colorectal cancer tissues (p=0.004). Similarly, the negative correlation between SM22 and p62 was verified in human CRC cell lines. The data suggest that the autophagy activity decreased in human CRC, which was associated with reduction in SM22 expression. However, the expression of SM22 was not associated with the gender, tumor site and Duke's stage of the patients. In conclusion, our findings suggest that the disruption of SM22 may be involved in tumorigenesis in CRC. The autophagic activity may be suppressed in human CRC, and SM22 may act as a positive regulator in the processes of autophagy.
Insights
Colorectal cancer (CRC) shows reduced SM22 protein levels, correlating with decreased autophagy. This suggests SM22 disruption may drive CRC tumorigenesis by suppressing autophagy.
Area of Science:
- Oncology
- Molecular Biology
- Cellular Biology
Background:
- Colorectal cancer (CRC) is a significant global health concern with high mortality.
- Autophagy deregulation is increasingly recognized in human cancer development.
- SM22 is identified as a potential tumor suppressor protein.
Purpose of the Study:
- To investigate the relationship between SM22 expression and autophagy activity in colorectal cancer.
- To explore the correlation between SM22 levels and clinical characteristics of CRC patients.
Main Methods:
- Western blot and immunohistochemical staining were used to detect SM22 and p62 (autophagy biomarker) expression.
- Paired tumor and adjacent non-tumor tissues from 43 CRC patients were analyzed.
- Expression analysis was also performed in human CRC cell lines.
Main Results:
- SM22 expression was significantly decreased in 81.4% of CRC tissues.
- p62 expression was elevated in 79.1% of CRC tissues, indicating increased autophagy activity.
- A significant negative correlation was found between SM22 and p62 expression in CRC tissues and cell lines (p=0.004).
Conclusions:
- Autophagy activity appears suppressed in human colorectal cancer, linked to reduced SM22 expression.
- SM22 disruption may contribute to CRC tumorigenesis.
- SM22 may function as a positive regulator of autophagy in the context of CRC.
Related Concept Videos
Autophagy
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
Abnormal Proliferation

