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Updated: Jun 18, 2026

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
Published on: January 22, 2018
Ectopic expression of guanylyl cyclase C in gastric cancer as a potential biomarker and therapeutic target
Zhen Biao Mao1, Jian Feng Zhang, Zhong Xu
1Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, China. mzb63@163.com
Objective:
To investigate the expression of guanylyl cyclase C (GCC) in human gastric cancer (GC) tissues and assess the effect of GCC small interfering RNA (siRNA) on the proliferation and apoptosis of SGC-7901.
Methods:
The expression of GCC in 30 specimens and three human GC cell lines (SGC-7901, AGS, NCI-N87) were detected by RT-PCR for messenger RNA (mRNA) by Western blot and immunofluorescence for proteins. Recombinant plasmids containing GCC siRNA and scrambled siRNA were constructed and transfected into SGC-7901 cells, respectively. A cell counting kit-8, flow cytometry (FCM) and terminal deoxynucleotidyl transferase (TDT)-mediated dUTP-biotin nick end-labeling were used to evaluate cell viability, cell cycle distribution and apoptosis, followed by wound healing assay and cell adherent assay for cell motility and adherent, respectively.
Results:
The expression of GCC was absent in paracancerous tissues, whereas the GCC mRNA and protein expressions were detected in 20/30 and 19/30 of GC specimens, respectively. Moreover, intestinal GC was statistically different from diffuse GC (P < 0.05). The proliferation of SGC-7901 cells was markedly inhibited by GCC siRNA-3 (P < 0.05) and cell morphological changes including volumetric reduction, karyopyknosis and karyorrhexis were observed. FCM showed that the cell count in the sub-G0/G1 peak increased from 5.47% (48 h after transfection) to 5.63% (72 h after transfection). The wound healing assay and cell adherent assay revealed that GCC gene silencing decreased cell motility and adherent.
Conclusion:
The over-expression of GCC has been detected in intestinal type GC. GCC siRNA can effectively inhibit the proliferation and invasion of SGC-7901 cells and induce cell apoptosis. GCC might be a novel biomarker and therapeutic target for GC.
Insights
Guanylyl cyclase C (GCC) is overexpressed in intestinal gastric cancer (GC). GCC small interfering RNA (siRNA) effectively inhibits GC cell proliferation and invasion while inducing apoptosis, suggesting GCC as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Guanylyl cyclase C (GCC) is a transmembrane receptor guanylyl cyclase.
- Its role in gastric cancer (GC) pathogenesis and progression is not fully understood.
Purpose of the Study:
- To investigate GCC expression in human GC tissues.
- To evaluate the impact of GCC small interfering RNA (siRNA) on SGC-7901 cell proliferation and apoptosis.
Main Methods:
- GCC expression (mRNA and protein) was assessed in GC specimens and cell lines using RT-PCR, Western blot, and immunofluorescence.
- SGC-7901 cells were transfected with GCC siRNA or scrambled siRNA.
- Cell proliferation, apoptosis, cell cycle, motility, and adhesion were evaluated using CCK-8, FCM, TUNEL, wound healing, and cell adhesion assays.
Main Results:
- GCC expression was detected in 20/30 GC specimens but absent in adjacent tissues, with higher prevalence in intestinal GC.
- GCC siRNA significantly inhibited SGC-7901 cell proliferation, induced apoptosis, and reduced cell motility and adhesion.
- Morphological changes indicative of apoptosis were observed in treated cells.
Conclusions:
- GCC is overexpressed in intestinal-type GC, indicating its potential as a biomarker.
- GCC siRNA demonstrates efficacy in inhibiting GC cell proliferation and invasion and inducing apoptosis.
- GCC represents a promising novel therapeutic target for gastric cancer.
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