Illustration of SP-D protein halting the spread of pancreatic cancer cells.

Cracking the Cancer Code: How a Lung Protein Could Stop Pancreatic Tumors in Their Tracks

Avery Sinclair in Health & Wellness November 2025 • 4 min read.

"New research reveals the surprising power of surfactant protein D (SP-D) in suppressing the spread of pancreatic cancer by targeting a key process called epithelial-to-mesenchymal transition (EMT)."

Pancreatic cancer remains one of the most aggressive and challenging cancers to treat. With a dismal five-year survival rate, researchers worldwide are tirelessly searching for new ways to combat this disease. One promising avenue involves understanding and targeting the process of metastasis—how cancer cells spread from the primary tumor to other parts of the body.

A critical step in metastasis is the epithelial-to-mesenchymal transition (EMT). EMT allows cancer cells to break free from the original tumor, migrate, and invade new tissues. Scientists are working hard to identify factors that can block or reverse EMT, potentially halting the spread of cancer.

Now, a groundbreaking study is shedding light on an unexpected player in the fight against pancreatic cancer: a protein called surfactant protein D (SP-D). Normally found in the lungs, SP-D plays a key role in the immune system. Researchers have discovered that SP-D can suppress EMT in pancreatic cancer cells, potentially offering a new strategy to slow or stop the disease's progression.

How Does SP-D Stop Cancer Cells From Spreading?

Illustration of SP-D protein halting the spread of pancreatic cancer cells.

The study, conducted by Anuvinder Kaur, Muhammad Suleman Riaz, Shiv K. Singh, and Uday Kishore, investigated the effects of a recombinant fragment of human SP-D (rfhSP-D) on pancreatic cancer cells. The results were remarkable: rfhSP-D effectively suppressed the invasive-mesenchymal properties of highly aggressive pancreatic cancer cells.

The key to SP-D's anti-cancer activity lies in its ability to target a signaling pathway known as TGF-β (Transforming Growth Factor beta). TGF-β is a cytokine (cell signaling molecule) that promotes EMT, but SP-D interferes with TGF-β's actions, preventing cancer cells from undergoing the transition that allows them to spread. Here’s what the study revealed:

Reduced TGF-β Expression: SP-D treatment significantly lowered the amount of TGF-β produced by pancreatic cancer cells.
Interrupted Smad Signaling: SP-D disrupted the signaling pathway that TGF-β uses to communicate with the cell's nucleus, preventing the activation of genes that drive EMT.
Downregulated Mesenchymal Genes: SP-D decreased the production of key proteins (Vimentin, Zeb1, and Snail) that are essential for EMT.
Reduced Invasion: SP-D significantly reduced the ability of pancreatic cancer cells to invade through a membrane mimicking tissue.

These findings demonstrate that SP-D acts as an innate immune surveillance molecule, actively interfering with EMT induction by attenuating the TGF-β pathway in pancreatic cancer.

What Does This Mean for the Future of Pancreatic Cancer Treatment?

This research opens exciting new possibilities for treating pancreatic cancer. By harnessing the power of SP-D to block EMT, scientists may be able to develop therapies that prevent the spread of the disease and improve patient outcomes. Further studies are needed to explore how SP-D can be effectively delivered to tumors and to identify patients who are most likely to benefit from this approach.

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: 10.3389/fimmu.2018.01844, Alternate LINK

Title: Human Surfactant Protein D Suppresses Epithelial-To-Mesenchymal Transition In Pancreatic Cancer Cells By Downregulating Tgf-Β

Subject: Immunology

Journal: Frontiers in Immunology

Publisher: Frontiers Media SA

Authors: Anuvinder Kaur, Muhammad Suleman Riaz, Shiv K. Singh, Uday Kishore

Published: 2018-08-15

Everything You Need To Know

What is surfactant protein D (SP-D), and how does it relate to pancreatic cancer?

Surfactant protein D (SP-D) is a protein normally found in the lungs. It has been discovered to suppress epithelial-to-mesenchymal transition (EMT) in pancreatic cancer cells, potentially preventing the spread of the disease. It achieves this by targeting a signaling pathway known as TGF-β (Transforming Growth Factor beta).

What is epithelial-to-mesenchymal transition (EMT), and why is it important in the context of cancer?

Epithelial-to-mesenchymal transition (EMT) is a critical step in metastasis, the process by which cancer cells spread from the primary tumor to other parts of the body. During EMT, cancer cells break free from the original tumor, migrate, and invade new tissues. Blocking or reversing EMT is a key strategy in preventing cancer from spreading. Disrupting EMT can prevent cancer cells from invading new tissues.

How exactly does surfactant protein D (SP-D) prevent the spread of pancreatic cancer at the molecular level?

SP-D targets the TGF-β (Transforming Growth Factor beta) signaling pathway, a cytokine that promotes EMT. Specifically, SP-D reduces the amount of TGF-β produced by pancreatic cancer cells, interrupts the Smad signaling pathway that TGF-β uses to communicate with the cell's nucleus, and downregulates the production of key proteins like Vimentin, Zeb1, and Snail that are essential for EMT. By interfering with the TGF-β pathway, SP-D prevents cancer cells from undergoing the transition that allows them to spread.

What are the potential implications of these findings for the future treatment of pancreatic cancer?

The research suggests that SP-D could be used to develop therapies that prevent the spread of pancreatic cancer by blocking EMT. This could potentially improve patient outcomes for this aggressive and challenging cancer. Further studies are needed to determine how SP-D can be effectively delivered to tumors and to identify which patients are most likely to benefit from this approach. Research is also needed to determine appropriate does and toxicity thresholds.

What specific form of SP-D was used in the study, and who conducted the research?

The study used a recombinant fragment of human SP-D (rfhSP-D) to investigate the effects of SP-D on pancreatic cancer cells. The researchers, Anuvinder Kaur, Muhammad Suleman Riaz, Shiv K. Singh, and Uday Kishore, found that rfhSP-D effectively suppressed the invasive-mesenchymal properties of highly aggressive pancreatic cancer cells. This suggests that a similar recombinant form of SP-D could be used in future therapies.