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Penicillin‑binding protein 1A mutation‑positive Helicobacter pylori promotes epithelial‑mesenchymal transition in gastric cancer via the suppression of microRNA‑134

  • Authors:
    • Lu Huang
    • Zhi‑Yong Wang
    • Dao‑Dong Pan

  • View Affiliations

  • Published online on: December 12, 2018     https://doi.org/10.3892/ijo.2018.4665
  • Pages: 916-928

  • Copyright: © Huang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Evidence suggests that Helicobacter pylori (H. pylori) is not only the main cause of gastric cancer (GC), but is also closely associated with its metastasis. One of the major virulence factors in H. pylori is the cytotoxin‑associated gene A (CagA). With the growing proportion of amoxicillin‑resistant H. pylori strains, the present study aimed to explore the effects of CagA‑ and penicillin‑binding protein 1A (PBP1A) mutation‑positive H. pylori (H. pyloriCagA+/P+) on GC cells, and its clinical significance. The clinical significance of H. pyloriCagA+/P+ infection was analyzed in patients with GC. In vitro, GC cells were infected with H. pyloriCagA+/P+ to investigate whether it was involved in the epithelial‑mesenchymal transition (EMT) of SGC‑7901 cells using immunofluorescence and western blot analysis. The results of clinical analysis demonstrated that, although CagA‑negative H. pylori infection had no significant association with the characteristics of patients with GC, H. pyloriCagA+/P+ infection was significantly associated with various clinicopathological parameters, including invasion depth, lymphatic metastasis and distant metastasis. In vitro, the results indicated that H. pyloriCagA+/P+ promoted proliferation, invasion and EMT of SGC‑7901 cells. MicroRNA (miR)‑134 was downregulated in H. pyloriCagA+/P+ infected tissues compared with in those with H. pyloriCagA+/P‑ infection. miR‑134 overexpression significantly reversed H. pyloriCagA+/P+ infection‑associated cell proliferation, invasion and EMT. Furthermore, the results revealed that Forkhead box protein M1 (FoxM1) was a direct target of miR‑134, and FoxM1 knockdown impeded H. pyloriCagA+/P+‑induced EMT. In conclusion, the present study demonstrated that miR‑134 may suppress the proliferation, invasion and EMT of SGC‑7901 cells by targeting FoxM1, and may serve a protective role in the process of H. pyloriCagA+/P+‑induced GC. These findings may lead to an improved understanding of H. pyloriCagA+/P+‑associated poor clinical characteristics in patients with GC.
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March-2019
Volume 54 Issue 3

Print ISSN: 1019-6439
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Spandidos Publications style
Huang L, Wang ZY and Pan DD: Penicillin‑binding protein 1A mutation‑positive Helicobacter pylori promotes epithelial‑mesenchymal transition in gastric cancer via the suppression of microRNA‑134. Int J Oncol 54: 916-928, 2019
APA
Huang, L., Wang, Z., & Pan, D. (2019). Penicillin‑binding protein 1A mutation‑positive Helicobacter pylori promotes epithelial‑mesenchymal transition in gastric cancer via the suppression of microRNA‑134. International Journal of Oncology, 54, 916-928. https://doi.org/10.3892/ijo.2018.4665
MLA
Huang, L., Wang, Z., Pan, D."Penicillin‑binding protein 1A mutation‑positive Helicobacter pylori promotes epithelial‑mesenchymal transition in gastric cancer via the suppression of microRNA‑134". International Journal of Oncology 54.3 (2019): 916-928.
Chicago
Huang, L., Wang, Z., Pan, D."Penicillin‑binding protein 1A mutation‑positive Helicobacter pylori promotes epithelial‑mesenchymal transition in gastric cancer via the suppression of microRNA‑134". International Journal of Oncology 54, no. 3 (2019): 916-928. https://doi.org/10.3892/ijo.2018.4665