Related Experiment Video

Updated: Feb 10, 2026

Multianimal Magnetic Resonance Imaging for Tumor Measurements in Pancreatic Cancer Mouse Models
09:18

Multianimal Magnetic Resonance Imaging for Tumor Measurements in Pancreatic Cancer Mouse Models

Published on: February 3, 2026

191

Natural compound Oblongifolin C confers gemcitabine resistance in pancreatic cancer by downregulating Src/MAPK/ERK

Yang Li1,2, Zhichao Xi1,2, Xiaoqiong Chen1,2

  • 1School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, P. R. China.

Cell Death & Disease
|May 12, 2018
PubMed

Insights

Oblongifolin C (OC) overcomes gemcitabine (GEM)-resistant pancreatic cancer (PC) by degrading Src and downregulating the MAPK pathway. OC re-sensitizes resistant PC cells, inhibiting tumor growth and enhancing chemotherapy effectiveness.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Gemcitabine (GEM) resistance is a significant challenge in pancreatic cancer (PC) chemotherapy.
  • Identifying novel therapeutic strategies to overcome drug resistance is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the efficacy of Oblongifolin C (OC) in overcoming gemcitabine (GEM)-induced drug resistance in pancreatic cancer (PC).
  • To elucidate the underlying molecular mechanisms by which OC re-sensitizes resistant PC cells.

Main Methods:

  • Cell proliferation assays, apoptosis assays, and cell cycle analysis were performed.
  • Mechanism studies involved investigating the role of Src and the MAPK pathway.
  • In vivo studies assessed tumor growth suppression and chemosensitivity enhancement.

Main Results:

  • Oblongifolin C (OC) inhibited PC cell proliferation by inducing G0/G1 arrest and apoptosis.
  • OC re-sensitized GEM-resistant PC cells via ubiquitin-proteasome-dependent degradation of Src, downregulating the MAPK pathway.
  • OC suppressed tumor growth in vivo and enhanced GEM chemosensitivity in resistant PC.

Conclusions:

  • Oblongifolin C (OC) demonstrates significant potential as a therapeutic agent to overcome gemcitabine (GEM)-induced resistance in pancreatic cancer (PC).
  • The mechanism involves Src degradation and MAPK pathway downregulation, offering a novel strategy for treating resistant PC, particularly with aberrant Src expression.

More Related Videos

Patient-derived Heterogeneous Xenograft Model of Pancreatic Cancer Using Zebrafish Larvae as Hosts for Comparative Drug Assessment09:56

Patient-derived Heterogeneous Xenograft Model of Pancreatic Cancer Using Zebrafish Larvae as Hosts for Comparative Drug Assessment

Published on: April 30, 2019

9.6K
Spatial and Temporal Analysis of Active ERK in the C. elegans Germline08:40

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline

Published on: November 29, 2016

10.8K

Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.8K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.9K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
8.5K
C4 Pathway and CAM01:27

C4 Pathway and CAM

Most plants use the C3 pathway for carbon fixation. However, some plants, such as sugar cane, corn, and cacti that grow in hot conditions, use alternative pathways to fix carbon and conserve energy loss due to photorespiration. Photorespiration is the process that occurs when the oxygen concentration is high. Under such conditions, the rubisco enzyme in the Calvin cycle binds O2 instead of CO2, which halts photosynthesis and consumes energy.
C4 Pathway
The C4 pathway is used by plants such as...
49.3K
Nature and Nurture01:10

Nature and Nurture

Many human characteristics, like height, are shaped by both nature—in other words, by our genes—and by nurture, or our environment. For example, chronic stress during childhood inhibits the production of growth hormones and consequently reduces bone growth and height. Scientists estimate that 70-90% of variation in height is due to genetic differences among individuals, and 10-30% of variation in height is due to differences in the environments that individuals experience,...
22.4K
Molecules and Compounds02:38

Molecules and Compounds

Atoms and Molecules
69.2K