RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cells
Abstract Introduction The purpose of this research was to determine how the P53/microRNA‐34a (miR‐34a)/survivin pathway contributes to oxaliplatin‐induced (L‐OHP) cell inhibition in gastric cancer. Methods The BGC‐823 gastric cancer cells were selected, and we examined their viability following trea...
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| Format: | Article |
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Wiley
2024-09-01
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| Series: | Immunity, Inflammation and Disease |
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| Online Access: | https://doi.org/10.1002/iid3.70004 |
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| author | Qiang Guo Xin‐Yuan Wang Yan‐Chang Zhai Yong‐Wei Dong Qing‐Si He |
| author_facet | Qiang Guo Xin‐Yuan Wang Yan‐Chang Zhai Yong‐Wei Dong Qing‐Si He |
| author_sort | Qiang Guo |
| collection | DOAJ |
| description | Abstract Introduction The purpose of this research was to determine how the P53/microRNA‐34a (miR‐34a)/survivin pathway contributes to oxaliplatin‐induced (L‐OHP) cell inhibition in gastric cancer. Methods The BGC‐823 gastric cancer cells were selected, and we examined their viability following treatment with L‐OHP at different concentrations and time periods. The expression levels of miR‐34a, P53, and survivin in the cells were determined. Results In the 12‐ and 24‐h groups, drug concentration of 15 μg/cm² (p < .005 in both) significantly lowered cell viability. In comparison to the control group, miR‐34a mRNA expression, P53 mRNA expression, and protein expression were all significantly greater in the 24‐h group (p = .0324, p = .0069, p = .0260, respectively), but survivin mRNA and protein expressions were significantly lower than those in the control group (p = .0338, p = .0032, respectively). There was a significant decrease in gastric cancer cells in the miR‐34a overexpression group (p = .0020), a significant increase in P53 mRNA and protein expression compared to the control group (p = .0080, p = .0121, respectively), and a significant decrease in survivin mRNA and protein expression compared to the control group. (p = .0213, p = .0069, respectively). Conclusion Oxaliplatin inhibits tumor growth, invasion, and metastasis by upregulating miR‐34a, activating the expression of the upstream P53 gene, and driving the downregulation of survivin (P53/miR‐34a/survivin axis) in BGC‐823 gastric cancer cells. |
| format | Article |
| id | doaj-art-ee9cbbb0db6d44ee9df4c0bdb1341e58 |
| institution | DOAJ |
| issn | 2050-4527 |
| language | English |
| publishDate | 2024-09-01 |
| publisher | Wiley |
| record_format | Article |
| series | Immunity, Inflammation and Disease |
| spelling | doaj-art-ee9cbbb0db6d44ee9df4c0bdb1341e582025-08-20T03:08:21ZengWileyImmunity, Inflammation and Disease2050-45272024-09-01129n/an/a10.1002/iid3.70004RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cellsQiang Guo0Xin‐Yuan Wang1Yan‐Chang Zhai2Yong‐Wei Dong3Qing‐Si He4Department of Gastrointestinal Surgery The First Affiliated Hospital of Baotou Medical College Baotou ChinaDepartment of General Surgery HeNan RongJun Hospital Xinxiang ChinaDepartment of Gastrointestinal Surgery Qi Lu Hospital of Shandong University Jinan ChinaDepartment of Gastrointestinal Surgery Qi Lu Hospital of Shandong University Jinan ChinaDepartment of Gastrointestinal Surgery The First Affiliated Hospital of Baotou Medical College Baotou ChinaAbstract Introduction The purpose of this research was to determine how the P53/microRNA‐34a (miR‐34a)/survivin pathway contributes to oxaliplatin‐induced (L‐OHP) cell inhibition in gastric cancer. Methods The BGC‐823 gastric cancer cells were selected, and we examined their viability following treatment with L‐OHP at different concentrations and time periods. The expression levels of miR‐34a, P53, and survivin in the cells were determined. Results In the 12‐ and 24‐h groups, drug concentration of 15 μg/cm² (p < .005 in both) significantly lowered cell viability. In comparison to the control group, miR‐34a mRNA expression, P53 mRNA expression, and protein expression were all significantly greater in the 24‐h group (p = .0324, p = .0069, p = .0260, respectively), but survivin mRNA and protein expressions were significantly lower than those in the control group (p = .0338, p = .0032, respectively). There was a significant decrease in gastric cancer cells in the miR‐34a overexpression group (p = .0020), a significant increase in P53 mRNA and protein expression compared to the control group (p = .0080, p = .0121, respectively), and a significant decrease in survivin mRNA and protein expression compared to the control group. (p = .0213, p = .0069, respectively). Conclusion Oxaliplatin inhibits tumor growth, invasion, and metastasis by upregulating miR‐34a, activating the expression of the upstream P53 gene, and driving the downregulation of survivin (P53/miR‐34a/survivin axis) in BGC‐823 gastric cancer cells.https://doi.org/10.1002/iid3.70004gastric cancermiR‐34aoxaliplatinP53 genesurvivin gene |
| spellingShingle | Qiang Guo Xin‐Yuan Wang Yan‐Chang Zhai Yong‐Wei Dong Qing‐Si He RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cells Immunity, Inflammation and Disease gastric cancer miR‐34a oxaliplatin P53 gene survivin gene |
| title | RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cells |
| title_full | RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cells |
| title_fullStr | RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cells |
| title_full_unstemmed | RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cells |
| title_short | RETRACTED: Oxaliplatin activates P53/miR‐34a/survivin axis in inhibiting the progression of gastric cancer cells |
| title_sort | retracted oxaliplatin activates p53 mir 34a survivin axis in inhibiting the progression of gastric cancer cells |
| topic | gastric cancer miR‐34a oxaliplatin P53 gene survivin gene |
| url | https://doi.org/10.1002/iid3.70004 |
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