Pseudogene BNIP3P1 Regulates H. pylori–Induced Apoptosis in Gastric Mucosal by Acting on the miR‐411‐5p/BNIP3 Axis Article Swipe
YOU?
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· 2025
· Open Access
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· DOI: https://doi.org/10.1155/cmi/6763794
Helicobacter pylori ( H. pylori ) is one of the major causes of gastric mucosal damage, and infection with H. pylori induces an immune response with gastric mucosal cells, which reduces gastric mucosal damage. The pseudogene BNIP3P1 , sharing a remarkable 95.92% similarity with its well‐characterized counterpart BNIP3 , has largely remained unexplored. To elucidate the role of BNIP3P1 in gastric mucosal damage induced by H. pylori infection, we meticulously constructed both in vivo and in vitro models. Gene chip sequencing, dual‐luciferase assays, and cellular phenotyping were detected. We uncovered a compelling positive correlation between the duration of H. pylori infection and BNIP3 overexpression at both the mRNA and protein levels. Intriguingly, overexpression of BNIP3 was found to effectively impede the proliferation and migration of human gastric epithelial cells (GES‐1). Furthermore, we identified miR-411-5p as a direct regulator of BNIP3 , targeting its 3 ′ UTR region and suppressing its expression during H. pylori infection. Notably, BNIP3P1- 3 ′ UTR was observed to competitively bind miR-411-5p , leading to the upregulation of BNIP3 expression. Furthermore, overexpression of BNIP3P1 was associated with a marked decrease in GES‐1 cell proliferation and a concomitant acceleration of apoptosis. Our findings suggest that BNIP3P1 functions as a competing endogenous RNA (ceRNA) within the BNIP3/miR-411-5p axis during H. pylori infection, which ultimately hinders cell proliferation and promotes apoptosis in GES‐1 cells. This study sheds light on the intricate mechanisms underlying H. pylori infection of GES‐1 cells.
Related Topics
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1155/cmi/6763794
- https://onlinelibrary.wiley.com/doi/pdfdirect/10.1155/cmi/6763794
- OA Status
- gold
- References
- 34
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4410777700
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4410777700Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1155/cmi/6763794Digital Object Identifier
- Title
-
Pseudogene BNIP3P1 Regulates H. pylori–Induced Apoptosis in Gastric Mucosal by Acting on the miR‐411‐5p/BNIP3 AxisWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-01-01Full publication date if available
- Authors
-
Andong Zhang, Xin Yan, Ningzhe Li, Shiying Yan, S. Li, Hua Yang, Yimeng Liu, Jian Zhang, Jia Wang, Jian Zhao, Mei CaoList of authors in order
- Landing page
-
https://doi.org/10.1155/cmi/6763794Publisher landing page
- PDF URL
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1155/cmi/6763794Direct link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://onlinelibrary.wiley.com/doi/pdfdirect/10.1155/cmi/6763794Direct OA link when available
- Concepts
-
Pseudogene, Biology, Apoptosis, Cell biology, Cancer research, Genetics, Gene, GenomeTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- References (count)
-
34Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.BNIP3 | 47, 102, 114, 139, 172 |
| abstract_inverted_index.cells | 128 |
| abstract_inverted_index.found | 116 |
| abstract_inverted_index.human | 125 |
| abstract_inverted_index.light | 228 |
| abstract_inverted_index.major | 10 |
| abstract_inverted_index.sheds | 227 |
| abstract_inverted_index.study | 226 |
| abstract_inverted_index.vitro | 76 |
| abstract_inverted_index.which | 29, 214 |
| abstract_inverted_index.95.92% | 41 |
| abstract_inverted_index.causes | 11 |
| abstract_inverted_index.cells, | 28 |
| abstract_inverted_index.cells. | 224, 239 |
| abstract_inverted_index.damage | 62 |
| abstract_inverted_index.direct | 136 |
| abstract_inverted_index.during | 151, 210 |
| abstract_inverted_index.immune | 23 |
| abstract_inverted_index.impede | 119 |
| abstract_inverted_index.marked | 182 |
| abstract_inverted_index.pylori | 1, 4, 20, 66, 99, 153, 212, 235 |
| abstract_inverted_index.region | 146 |
| abstract_inverted_index.within | 206 |
| abstract_inverted_index.(ceRNA) | 205 |
| abstract_inverted_index.BNIP3P1 | 36, 58, 177, 198 |
| abstract_inverted_index.GES‐1 | 185, 223, 238 |
| abstract_inverted_index.assays, | 82 |
| abstract_inverted_index.between | 94 |
| abstract_inverted_index.damage, | 15 |
| abstract_inverted_index.damage. | 33 |
| abstract_inverted_index.gastric | 13, 26, 31, 60, 126 |
| abstract_inverted_index.hinders | 216 |
| abstract_inverted_index.induced | 63 |
| abstract_inverted_index.induces | 21 |
| abstract_inverted_index.largely | 50 |
| abstract_inverted_index.leading | 167 |
| abstract_inverted_index.levels. | 110 |
| abstract_inverted_index.models. | 77 |
| abstract_inverted_index.mucosal | 14, 27, 32, 61 |
| abstract_inverted_index.protein | 109 |
| abstract_inverted_index.reduces | 30 |
| abstract_inverted_index.sharing | 38 |
| abstract_inverted_index.suggest | 196 |
| abstract_inverted_index.BNIP3P1- | 156 |
| abstract_inverted_index.Notably, | 155 |
| abstract_inverted_index.cellular | 84 |
| abstract_inverted_index.decrease | 183 |
| abstract_inverted_index.duration | 96 |
| abstract_inverted_index.findings | 195 |
| abstract_inverted_index.observed | 161 |
| abstract_inverted_index.positive | 92 |
| abstract_inverted_index.promotes | 220 |
| abstract_inverted_index.remained | 51 |
| abstract_inverted_index.response | 24 |
| abstract_inverted_index.apoptosis | 221 |
| abstract_inverted_index.competing | 202 |
| abstract_inverted_index.detected. | 87 |
| abstract_inverted_index.elucidate | 54 |
| abstract_inverted_index.functions | 199 |
| abstract_inverted_index.infection | 17, 100, 236 |
| abstract_inverted_index.intricate | 231 |
| abstract_inverted_index.migration | 123 |
| abstract_inverted_index.regulator | 137 |
| abstract_inverted_index.targeting | 141 |
| abstract_inverted_index.uncovered | 89 |
| abstract_inverted_index.(GES‐1). | 129 |
| abstract_inverted_index.apoptosis. | 193 |
| abstract_inverted_index.associated | 179 |
| abstract_inverted_index.compelling | 91 |
| abstract_inverted_index.endogenous | 203 |
| abstract_inverted_index.epithelial | 127 |
| abstract_inverted_index.expression | 150 |
| abstract_inverted_index.identified | 132 |
| abstract_inverted_index.infection, | 67, 213 |
| abstract_inverted_index.infection. | 154 |
| abstract_inverted_index.mechanisms | 232 |
| abstract_inverted_index.miR-411-5p | 133, 165 |
| abstract_inverted_index.pseudogene | 35 |
| abstract_inverted_index.remarkable | 40 |
| abstract_inverted_index.similarity | 42 |
| abstract_inverted_index.ultimately | 215 |
| abstract_inverted_index.underlying | 233 |
| abstract_inverted_index.concomitant | 190 |
| abstract_inverted_index.constructed | 70 |
| abstract_inverted_index.correlation | 93 |
| abstract_inverted_index.counterpart | 46 |
| abstract_inverted_index.effectively | 118 |
| abstract_inverted_index.expression. | 173 |
| abstract_inverted_index.phenotyping | 85 |
| abstract_inverted_index.sequencing, | 80 |
| abstract_inverted_index.suppressing | 148 |
| abstract_inverted_index.unexplored. | 52 |
| abstract_inverted_index.Furthermore, | 130, 174 |
| abstract_inverted_index.Helicobacter | 0 |
| abstract_inverted_index.acceleration | 191 |
| abstract_inverted_index.meticulously | 69 |
| abstract_inverted_index.upregulation | 170 |
| abstract_inverted_index.Intriguingly, | 111 |
| abstract_inverted_index.competitively | 163 |
| abstract_inverted_index.proliferation | 121, 187, 218 |
| abstract_inverted_index.overexpression | 103, 112, 175 |
| abstract_inverted_index.BNIP3/miR-411-5p | 208 |
| abstract_inverted_index.dual‐luciferase | 81 |
| abstract_inverted_index.well‐characterized | 45 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 11 |
| citation_normalized_percentile.value | 0.31004897 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |