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The influence of TXNDC5 gene on gastric cancer cell
Lin Zhang1, Yanhong Hou, Nan Li
1Department of Gastroenterology and Hepatology, The 309 Hospital of PLA, Beijing 100091, China. stepinghuns@yahoo.com.cn
Background:
TXNDC5 (thioredoxin domain containing 5) is over-expressed in tumors of the cervix, uterus, stomach and lung. However, not much is known about the functional roles of TXNDC5 gene in gastric adenocarcinoma. In the present study, we intend to investigate the effects of TXNDC5 on the growth, proliferation, apoptosis, invasion and cell cycle of the gastric cancer cell line MKN45 and normal gastric cell line HFE145.
Methods:
TXNDC5 cDNA was inserted into a constitutive vector pcDNA3.1 followed by transfection into normal gastric cell line HFE145 using liposome. Then, stable transfectants were selected and appraised. Specific silencing of TXNDC5 gene was achieved using a vector-based short interference RNAs (siRNA) system in gastric cancer cell line MKN45. The growth and proliferation were analyzed by cell growth curves and colony-forming assay, respectively. The apoptosis and cell cycles of these clones were analyzed using flow cytometry. The invasion of these cells was analyzed by cell migration assay. The TXNDC5 stable expression cell lines (HFE-TXNDC5) and TXNDC5 RNAi cell lines (MKN-SR1,2) were detected and compared with their control groups, respectively.
Results:
HFE-TXNDC5 grew faster than HFE145 and HFE-PC(HFE145 transfected with pcDNA3.1 vector). MKN-SR1 grew slower than MKN45 and MKN-SS1,2 (MKN45 transfected with scrambled control duplexes). The cell counts of HFE-TXNDC5 in the fifth, sixth and seventh days were significantly higher than those of control groups (P < 0.05). The cell counts of MKN-SR1 in the fifth, sixth and seventh days were significantly lower than those of control groups (P < 0.05). Cell cycle analysis showed that there were significant differences in proportions of G0-G1 and G2-M phase between HFE-TXNDC5, MKN-SR1 cells and their control groups, respectively (P < 0.05). The apoptosis rate of HFE-TXNDC5 was significantly lower than that of control groups (P < 0.05). The results of colony-forming assay showed that the colony formation rate of HFE-TXNDC5 was higher than those of control groups, otherwise the rate of MKN-SR1 were lower than those of their control groups (P < 0.05). The results of cell migration assay showed that the migration rate of HFE-TXNDC5 were significantly higher than that of its control group. Conversely, the migration rate of MKN-SR1 was significantly lower than that of its control group (P < 0.05).
Conclusion:
TXNDC5 can promote the growth and proliferation of gastric cells. Silencing of TXNDC5 can restrain the growth and proliferation of gastric cancer cells. The gene can enhance the capability of invasion of gastric cancer cells. In some respects, TXNDC5 could be thought as a tumor-enhancing gene in gastric cancer.
Insights
Thioredoxin domain containing 5 (TXNDC5) promotes gastric cell growth, proliferation, and invasion. Silencing TXNDC5 restrains gastric cancer cell growth, indicating its role as a tumor-enhancing gene.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- TXNDC5 is over-expressed in various cancers, including gastric adenocarcinoma.
- The specific functional roles of TXNDC5 in gastric cancer remain largely unknown.
- This study investigates TXNDC5's impact on gastric cancer cell behavior.
Purpose of the Study:
- To elucidate the functional significance of TXNDC5 in gastric adenocarcinoma.
- To determine TXNDC5's effects on gastric cell growth, proliferation, apoptosis, invasion, and cell cycle.
- To evaluate TXNDC5 as a potential therapeutic target in gastric cancer.
Main Methods:
- TXNDC5 gene was overexpressed in normal gastric cells (HFE145) and silenced in gastric cancer cells (MKN45) using siRNA.
- Cell growth, proliferation, apoptosis, cell cycle, and invasion were assessed.
- Stable cell lines (HFE-TXNDC5 and MKN-SR1) were generated and compared to control groups.
Main Results:
- Overexpression of TXNDC5 in HFE145 cells accelerated growth and proliferation.
- Silencing TXNDC5 in MKN45 cells inhibited growth and proliferation.
- TXNDC5 influenced cell cycle distribution and reduced apoptosis in normal cells.
- TXNDC5 overexpression enhanced cell invasion, while silencing reduced it in cancer cells.
Conclusions:
- TXNDC5 promotes gastric cell growth, proliferation, and invasion.
- Silencing TXNDC5 inhibits gastric cancer cell progression.
- TXNDC5 functions as a tumor-enhancing gene in gastric cancer.
- Targeting TXNDC5 may offer a therapeutic strategy for gastric adenocarcinoma.
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