Helicobacter pylori infection induces STAT3/MYBL2/NF-κB axis to promote gastric cancer progression

  • 0Research Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical University, Jinan 250013, PR China; Department of Medical Laboratory, Shandong Second Medical University, Weifang 261053, PR China.

|

|

Summary

This summary is machine-generated.

Helicobacter pylori infection increases MYBL2 expression, promoting gastric cancer (GC) cell growth and migration. Targeting this pathway may offer new strategies for treating H. pylori-associated GC.

Area Of Science

  • Oncology
  • Gastroenterology
  • Molecular Biology

Background

  • Helicobacter pylori (H. pylori) infection is a major risk factor for gastric cancer (GC).
  • The role of MYBL2 in H. pylori-induced GC progression remains under-investigated.
  • MYBL2 is implicated in the oncogenesis of various cancers.

Purpose Of The Study

  • To investigate the expression and clinical significance of MYBL2 in GC.
  • To elucidate the role of MYBL2 in H. pylori-mediated GC development.
  • To identify the molecular mechanisms linking H. pylori infection, MYBL2, and GC progression.

Main Methods

  • Analyzing MYBL2 expression in GC tissues and cell lines.
  • Inducing H. pylori infection in vitro and in vivo models.
  • Assessing the impact of MYBL2 modulation on GC cell proliferation, migration, and tumor growth in xenograft models.
  • Investigating the upstream and downstream signaling pathways involving STAT3, MYBL2, and NF-κB.

Main Results

  • H. pylori infection significantly upregulated MYBL2 expression in GC.
  • Downregulation of MYBL2 suppressed H. pylori-induced GC cell proliferation and migration.
  • MYBL2 promoted tumor growth in vivo.
  • H. pylori infection activated STAT3, leading to increased MYBL2 expression.
  • MYBL2 was identified as an upstream regulator of NF-κB activation in GC cells.

Conclusions

  • The H. pylori/STAT3/MYBL2/NF-κB signaling axis is crucial for regulating H. pylori-induced GC.
  • MYBL2 plays a significant role in the progression of gastric cancer associated with H. pylori infection.
  • Targeting the MYBL2 pathway presents a potential therapeutic strategy for H. pylori-related GC.

Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors 01:24

604

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.

Pathophysiology of Peptic Ulcer Disease: Injurious Factors 01:22

728

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...

Gastritis-II: Pathophysiology 01:17

601

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...

Abnormal Proliferation 02:23

4.6K

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Peptic Ulcer Disease I: Introduction 01:30

302

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...

NF-κB-dependent Signaling Pathway 02:26

7.9K

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...