Related Experiment Video

Updated: Jan 3, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

18.5K

Inhibition of PTP1B blocks pancreatic cancer progression by targeting the PKM2/AMPK/mTOC1 pathway

Qi Xu1,2,3, Ning Wu1,2, Xiangqian Li4,3

  • 1Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.

Cell Death & Disease
|November 21, 2019
PubMed

Insights

Protein-tyrosine phosphatase 1B (PTP1B) is highly expressed in pancreatic cancer, promoting tumor growth and metastasis. Inhibiting PTP1B suppressed pancreatic cancer progression by targeting the PKM2/AMPK/mTOC1 pathway, suggesting PTP1B as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Pancreatic cancer (PDAC) is a lethal malignancy with limited effective treatments.
  • Protein-tyrosine phosphatase 1B (PTP1B) is implicated in various diseases, but its role in PDAC is unclear.
  • PTP1B's dual role in tumorigenesis necessitates investigation in pancreatic cancer.

Purpose of the Study:

  • To investigate the role of PTP1B in pancreatic cancer progression.
  • To determine if PTP1B is a viable therapeutic target for PDAC.
  • To elucidate the molecular mechanisms by which PTP1B influences PDAC.

Main Methods:

  • Assessed PTP1B expression in pancreatic tumors and correlated it with clinical parameters.
  • Utilized shRNA and small-molecule inhibitors to block PTP1B activity in vitro and in vivo.
  • Performed mechanistic studies to identify signaling pathways regulated by PTP1B.

Main Results:

  • PTP1B expression was elevated in PDAC tissues and linked to metastasis, advanced staging, and poor survival.
  • PTP1B inhibition reduced cancer cell proliferation, migration, and colony formation, causing cell cycle arrest.
  • Inhibition of PTP1B suppressed tumor growth in vivo.
  • PTP1B regulates PDAC progression via the PKM2/AMPK/mTORC1 pathway.

Conclusions:

  • PTP1B acts as an oncogene in pancreatic cancer.
  • Targeting PTP1B demonstrates therapeutic potential for PDAC.
  • The PKM2/AMPK/mTORC1 pathway is a key mediator of PTP1B's oncogenic function in PDAC.

More Related Videos

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.2K
Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors08:45

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Published on: July 17, 2020

6.5K

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.2K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.6K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.1K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.5K
Abnormal Proliferation02:23

Abnormal Proliferation

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...
5.0K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
11.7K