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Updated: May 19, 2026

Spectrophotometric Screening for Potential Inhibitors of Cytosolic Glutathione S-Transferases
Published on: October 10, 2020
Expression patterns of carcinogen detoxifying genes (CYP1A1, GSTP1 & GSTT1) in HNC patients
Nosheen Masood1, Mahmood Akhtar Kayani
1Cancer Genetics Lab, Department of Biosciences, COMSATS Institute of Information Technology, Islamabad, Pakistan. nosheenmasood@hotmail.com
Abstract:
Carcinogen detoxifying genes may be involved in pathogenesis of head and neck cancer (HNC). CYP1A1 is phase I enzyme that converts carcinogens into water soluble compounds which are easily excreted from body. GSTs constitute phase II detoxification enzymes that recognize these highly electrophilic compounds and detoxify them. Abnormal expression of these genes can potentially lead to cancer initiation. In present study, we analyzed protein expression of these genes in a total of 192 HNC patients and noncancerous healthy control serum samples screened for GSTs specific activity by ELISA. Furthermore, expression of these molecules was also determined in 49 HNC tissues/ adjacent control tissue by immunohistochemistry with specific antibodies. Mean serum GSTs specific activity was found to be 7.7 (+11.5)U/L in HNC patients and 11.4 (+7.5)U/L in controls. Significant decrease (P < 0.05) in GSTs specific activity was observed in HNC patients compared with controls (P < 0.001). Data for immunohistochemistry showed that CYP1A1 and GSTT1 was down expressed whereas GSTP1 was over expressed in HNC tissues compared with adjacent normal control tissues. Results of immunohistochemistry revealed 63 % HNC tissues had weak, 27 % moderate and 10 % strong staining for CYP1A1. For GSTT1, 27 % HNC tissues had no staining, 49 % weak staining, 16 % moderate and 8 % strong staining. Similarly for GSTP1, percentages for weak, moderate and strong staining were 6 %, 12 % and 82 % respectively. These reduced proteins observed in cancer patients highlight a potential breach on DNA repair mechanism when compared with control. Thus altered expression of these detoxifying molecules may collectively contribute to HNC development in Pakistani population.
Insights
Head and neck cancer (HNC) patients show decreased activity of carcinogen-detoxifying enzymes like GSTs. Altered expression of CYP1A1, GSTT1, and GSTP1 in HNC tissues suggests a role in cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Carcinogen-detoxifying genes, including phase I (CYP1A1) and phase II (GSTs) enzymes, are crucial for metabolizing and excreting harmful compounds.
- Abnormal expression of these genes is implicated in the initiation and progression of various cancers, including head and neck cancer (HNC).
Purpose of the Study:
- To investigate the protein expression and activity of carcinogen-detoxifying enzymes (CYP1A1, GSTT1, GSTP1) in head and neck cancer (HNC) patients.
- To determine the association between the expression of these detoxifying molecules and HNC development in the Pakistani population.
Main Methods:
- Serum samples from 192 HNC patients and healthy controls were analyzed for GSTs specific activity using ELISA.
- Immunohistochemistry was employed to assess the protein expression of CYP1A1, GSTT1, and GSTP1 in 49 HNC tissues and adjacent non-cancerous tissues.
Main Results:
- Mean serum GSTs specific activity was significantly lower in HNC patients (7.7 U/L) compared to controls (11.4 U/L) (P < 0.001).
- Immunohistochemistry revealed down-regulation of CYP1A1 and GSTT1, and over-expression of GSTP1 in HNC tissues compared to adjacent normal tissues.
- Specific staining patterns indicated reduced CYP1A1 and GSTT1, and predominantly strong GSTP1 expression in HNC tissues.
Conclusions:
- Altered expression and activity of carcinogen-detoxifying enzymes, including CYP1A1, GSTT1, and GSTP1, are associated with head and neck cancer.
- These molecular changes may indicate a compromised DNA repair mechanism, contributing to HNC pathogenesis.
- The findings highlight the potential role of these detoxifying molecules in HNC development within the studied population.
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