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Published on: April 6, 2016
Effect of blocking IGF-I receptor on growth of human hepatocellular carcinoma cells
You-Cheng Zhang1, Xiao-Peng Wang, Ling-Yi Zhang
1Department of Surgery, Lanzhou University Second Hospital, Lanzhou 730030, Gansu Province, China. zhangychmd@yahoo.com.cn
Aim:
To study the expression level and localization of insulin-like growth factor -I receptor (IGF-IR) in HepG2 cells and Chang liver cells, and to observe the effect of anti-IGF-IR monoclonal antibody (alphaIR3) on the growth of HepG2 cells.
Methods:
The expression of IGF-IR in HepG2 cells and Chang liver cells was detected by immunohistochemistry. The influences of alphaIR3 on proliferation and apoptosis were examined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and electron microscopy, respectively. Flow cytometry (FCM) was applied for the analysis of cell cycle and apoptosis was observed under electron microscope.
Results:
IGF-IR was located in the membranes of both HepG2 and Chang liver cell lines, and the expression level of IGF-IR was higher in HepG2 cells than in Chang liver cells. Treated with 0.1 microg/mL alphaIR3 for 48 h in vitro, the cell growth index (GI) of HepG2 cells was significantly higher than that of control (103.41% vs 100%, P<0.01). However, the alphaIR3 for 24 h at final concentration of 4.0 microg/mL made the GI of HepG2 cells lower than that of control (93.37% vs 100%, P<0.01). Compared with control, treated with alphaIR3 for 48 h at final concentrations ranging from 1.0 microg/mL to 4.0 microg/mL markedly reduced the GIs of HepG2 cells (97.63%, 97.16%, 95.13%, 92.53% vs 100%, P<0.05 or P<0.01), treated with alphaIR3 for 72 h at final concentrations ranging from 0.2 microg/mL to 4.0 microg/mL decreased the GIs of HepG2 cells obviously (95%, 91.63%, 90.77%, 89.84%, 88.51% vs 100%, P<0.01), and treated with alphaIR3 for 96 h at final concentrations ranging from 0.5 microg/mL to 4.0 microg/mL made GIs of HepG2 cells lower significantly (88.86%, 83.97%, 79.81%, 77.24%, 70.51% vs 100%, P<0.05 or P<0.01). Moreover, treated with alphaIR3 from 24 h to 96 h at final concentrations ranging from 0.2 microg/mL to 4.0 microg/mL reduced the GI of HepG2 cells from 97.63% to 70.51% in a dose- and time-dependent manner. Also, alphaIR3 treatment for 72 h at final concentration from 0.5 microg/mL to 2.0 microg/mL increased the proportion of G0/G1 phase cells (61.73%, 67.1%, 83.7%, 76.87% vs 44.47%, P<0.01) and significantly decreased that of S phase cells (28.63%, 25.13%, 15.63%, 23.13% vs 53.17%, P<0.01), in contrast to the proportion of G2/M phase cells. The apoptotic rates of HepG2 cells were increased more than that of control (7.83%, 16.13%, 21.1%, 37.73% vs 4.13%, P<0.01).
Conclusion:
The malignant cell phenotype of human hepatocarcinoma cell is related to overexpression of IGF-IR. The blockage of IGF-IR with alphaIR3 may contribute to the inhibition of proliferation and induction of apoptosis in HepG2 cells.
Insights
The study found that insulin-like growth factor-I receptor (IGF-IR) is overexpressed in HepG2 liver cancer cells. Blocking IGF-IR with the monoclonal antibody alphaIR3 inhibits HepG2 cell proliferation and induces apoptosis, suggesting a therapeutic target.
Area of Science:
- Cell Biology
- Molecular Oncology
- Biochemistry
Background:
- Insulin-like growth factor-I receptor (IGF-IR) plays a critical role in cell growth and survival.
- Overexpression of IGF-IR is implicated in the malignant phenotype of various cancers, including hepatocarcinoma.
- Understanding IGF-IR expression and function in liver cancer cells is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression and localization of IGF-IR in HepG2 and Chang liver cells.
- To evaluate the anti-proliferative and pro-apoptotic effects of the anti-IGF-IR monoclonal antibody (alphaIR3) on HepG2 cells.
Main Methods:
- Immunohistochemistry was used to detect IGF-IR expression.
- The MTT assay assessed cell proliferation.
- Flow cytometry and electron microscopy were employed to analyze cell cycle and apoptosis.
- HepG2 and Chang liver cells were treated with varying concentrations and durations of alphaIR3.
Main Results:
- IGF-IR was localized to the cell membranes, with higher expression in HepG2 cells compared to Chang liver cells.
- alphaIR3 demonstrated a dose- and time-dependent inhibition of HepG2 cell growth.
- Treatment with alphaIR3 led to an increase in G0/G1 phase arrest and a significant induction of apoptosis in HepG2 cells.
Conclusions:
- The malignant phenotype of human hepatocarcinoma cells is associated with IGF-IR overexpression.
- Blocking IGF-IR with alphaIR3 shows potential in inhibiting proliferation and inducing apoptosis in HepG2 cells.
- Targeting IGF-IR represents a promising strategy for the treatment of hepatocarcinoma.
