Illustration of lung cancer cells being stopped from metastasizing.

Can Targeting This 'Off' Switch Slow Lung Cancer?

Nico Varela in Health & Wellness November 2025 • 4 min read.

"New Research Shows How Blocking PIGF May Disrupt Cancer Cell Growth"

Lung cancer remains one of the most formidable health challenges worldwide. While medical advancements continue, the complex nature of cancer cell behavior often requires multifaceted strategies. Recent studies are shedding light on how certain growth factors influence the spread of lung cancer, opening new avenues for potential treatments.

Among these growth factors, vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) have garnered attention. VEGF is well-known for its role in promoting blood vessel formation within tumors, facilitating their growth and spread. However, the specific role of PIGF in lung cancer metastasis—the process by which cancer cells spread to other parts of the body—has been less understood. But recent research suggests that PIGF plays a crucial role.

A new study published in Molecular Cell Biochemistry uncovers how PIGF signaling regulates the isoform splicing of vascular endothelial growth factor A, impacting lung cancer cell metastasis. The findings suggest that targeting PIGF could disrupt cancer cell growth and spread, offering a potential new therapeutic approach.

How PIGF Fuels Lung Cancer Spread: The Key Findings

Illustration of lung cancer cells being stopped from metastasizing.

The research team compared tissue samples from patients with non-small cell lung cancer (NSCLC) to healthy lung tissue. They discovered significantly higher levels of PIGF in NSCLC samples. What’s more, patients with distal metastases (cancer that has spread to distant sites) had even higher PIGF levels, suggesting a link between PIGF and cancer progression.

Further experiments revealed a correlation between high PIGF levels and poorer patient survival rates. This prompted the researchers to investigate how PIGF might be influencing cancer cell behavior at a molecular level.

Higher PIGF in Cancerous Tissues: NSCLC specimens showed significantly elevated PIGF levels compared to adjacent normal lung tissue.
Metastasis Link: Higher PIGF levels were detected in NSCLC specimens from patients with distal metastases, indicating a potential role in cancer spread.
Poor Survival Association: High PIGF levels appeared to be associated with reduced overall survival in NSCLC patients.

In laboratory experiments, the team found that PIGF influences the splicing of VEGF mRNA, leading to an increased ratio of pro-angiogenic VEGF isoforms (VEGF165) compared to anti-angiogenic isoforms (VEGF165b). This shift promotes blood vessel formation, which is essential for tumor growth and metastasis. They also discovered that PIGF's effect is mediated by a splicing regulatory factor called SRp40. Higher levels of SRp40 were found in NSCLC tissues, and a strong correlation was observed between PIGF and SRp40 levels. This suggests that PIGF increases NSCLC metastasis by modulating mRNA splicing of VEGF through SRp40.

The Future of Lung Cancer Treatment: Targeting PIGF

These findings suggest that PIGF is more than just a bystander in lung cancer; it actively promotes cancer cell spread. Targeting PIGF, or the SRp40 pathway it influences, could offer a new strategy to slow or prevent lung cancer metastasis. While more research is needed to develop effective PIGF-blocking therapies, this study provides a promising step forward in the fight against lung cancer.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1007/s11010-017-3145-3, Alternate LINK

Title: Placental Growth Factor Signaling Regulates Isoform Splicing Of Vascular Endothelial Growth Factor A In The Control Of Lung Cancer Cell Metastasis

Subject: Cell Biology

Journal: Molecular and Cellular Biochemistry

Publisher: Springer Science and Business Media LLC

Authors: Zanfeng Wang, Tingwei Liu

Published: 2017-08-31

Everything You Need To Know

What exactly is PIGF, and what role does it play?

PIGF, or placental growth factor, is a growth factor that plays a crucial role in lung cancer metastasis. Recent research suggests that blocking PIGF could disrupt cancer cell growth and spread. It's a protein that influences the behavior of cancer cells, specifically in the context of non-small cell lung cancer (NSCLC).

How does PIGF relate to VEGF, and what are the implications?

VEGF, or vascular endothelial growth factor, is a well-known growth factor that promotes blood vessel formation within tumors. PIGF influences the splicing of VEGF mRNA, leading to an increased ratio of pro-angiogenic VEGF isoforms (VEGF165) compared to anti-angiogenic isoforms (VEGF165b). This shift promotes blood vessel formation, which is essential for tumor growth and metastasis. The implications are that by modulating VEGF through PIGF, cancer progression is facilitated.

What does the term 'metastasis' mean in this context?

The term 'metastasis' refers to the process by which cancer cells spread from the primary tumor to other parts of the body. The research indicates that PIGF plays a crucial role in this process within the context of lung cancer. Patients with distal metastases showed even higher PIGF levels, suggesting a link between PIGF and cancer progression. The implications are that by targeting PIGF, the spread of cancer could potentially be slowed or stopped.

What is SRp40, and how does it connect to PIGF?

SRp40 is a splicing regulatory factor. Research found that PIGF's effect is mediated by SRp40. Higher levels of SRp40 were found in NSCLC tissues, and a strong correlation was observed between PIGF and SRp40 levels. This suggests that PIGF increases NSCLC metastasis by modulating mRNA splicing of VEGF through SRp40. The implication of this finding is that by targeting the SRp40 pathway influenced by PIGF, it could offer a new strategy to slow or prevent lung cancer metastasis.

Why is targeting PIGF considered significant in the fight against lung cancer?

The significance of targeting PIGF lies in its potential to slow or prevent lung cancer metastasis. The research suggests that blocking PIGF could disrupt cancer cell growth and spread. This is a promising step forward in the fight against lung cancer because it offers a new therapeutic approach. While more research is needed to develop effective PIGF-blocking therapies, this study provides a foundation for future treatments.