Microscopic view of cancer cells being neutralized by SRC-3 inhibitors.

Pancreatic Cancer Breakthrough: How SRC-3 Inhibition Could Change Everything

Reese Marlowe in Health & Wellness June 2025 • 4 min read.

"New research reveals SRC-3 as a key player in pancreatic cancer growth, offering hope for targeted therapies and improved survival rates."

Pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC), remains one of the most challenging and deadly cancers to treat. With a five-year survival rate of less than 8%, the need for new therapeutic approaches is urgent. Traditional treatments often fall short, highlighting the necessity for innovative strategies that target the unique characteristics of this aggressive disease.

Recent research has shed light on a promising new target: Steroid Receptor Coactivator-3 (SRC-3). This protein, involved in numerous growth-signaling pathways, has been identified as a key driver in the development and progression of PDAC. SRC-3's role in other cancers like breast and prostate has already been explored, but its significance in pancreatic cancer is just beginning to be understood.

This article delves into the groundbreaking findings regarding SRC-3 inhibition as a potential treatment for pancreatic cancer. We'll explore how scientists are targeting this protein to slow tumor growth, improve survival rates, and offer new hope to those affected by this devastating illness. By understanding the mechanisms behind SRC-3 and its impact on pancreatic cancer, we can pave the way for more effective and targeted therapies.

What is SRC-3 and Why Does It Matter in Pancreatic Cancer?

Microscopic view of cancer cells being neutralized by SRC-3 inhibitors.

SRC-3, also known as NCOA3, AIB1, pCIP, ACTR, RAC3, or TRAM1, is a protein that acts as a master regulator in numerous cellular processes. It influences a wide range of growth-signaling pathways, making it a crucial factor in cancer development. SRC-3's involvement in other cancers has led researchers to investigate its role in PDAC, where it appears to be significantly overexpressed.

The study found that SRC-3 is overexpressed in pancreatic ductal adenocarcinoma (PDAC) and inversely correlates with patient overall survival. This means higher levels of SRC-3 are associated with poorer outcomes for patients. Knocking down SRC-3 reduces pancreatic cancer cell proliferation, migration and invasion in vitro. Therefore, scientists believe that targeting SRC-3 could disrupt the growth and spread of cancer cells.

Cell Proliferation: SRC-3 promotes rapid cell division, a hallmark of cancer.
Migration: SRC-3 enhances the ability of cancer cells to move and spread.
Invasion: SRC-3 helps cancer cells penetrate surrounding tissues, facilitating metastasis.

These findings suggest that SRC-3 is not just a bystander but an active participant in the progression of pancreatic cancer. By understanding its role, researchers can develop targeted therapies to disrupt its functions and potentially halt or slow the disease's advancement.

The Future of Pancreatic Cancer Treatment: Hope on the Horizon

While the research on SRC-3 inhibition is still in its early stages, the results are promising. Targeting SRC-3 offers a new avenue for treating pancreatic cancer, potentially leading to improved survival rates and a better quality of life for patients. As research progresses, we can look forward to more effective, targeted therapies that address the unique challenges of this devastating disease. The journey is far from over, but the path toward hope is now clearer than ever.

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.

Everything You Need To Know

What is SRC-3, and why is it being researched as a potential target for pancreatic cancer treatment?

SRC-3, also known as NCOA3, AIB1, pCIP, ACTR, RAC3, or TRAM1, is a protein that acts as a master regulator in numerous cellular processes including growth-signaling pathways. Research suggests that SRC-3 is overexpressed in pancreatic ductal adenocarcinoma (PDAC), and higher levels of SRC-3 are associated with poorer survival outcomes. Scientists are exploring it as a therapeutic target because inhibiting SRC-3 could disrupt the growth and spread of pancreatic cancer cells.

In what specific ways does SRC-3 contribute to the progression of pancreatic cancer?

SRC-3 promotes pancreatic cancer progression through multiple mechanisms. It enhances cell proliferation, causing rapid cell division. It also increases cell migration, improving the ability of cancer cells to move and spread throughout the body. Finally, SRC-3 facilitates invasion, helping cancer cells penetrate surrounding tissues and leading to metastasis. Disrupting these functions of SRC-3 could potentially halt or slow the advancement of pancreatic cancer.

How does inhibiting SRC-3 impact pancreatic cancer cells in laboratory studies (in vitro)?

Studies have demonstrated that reducing or 'knocking down' SRC-3 in laboratory settings significantly reduces pancreatic cancer cell proliferation, migration, and invasion. This suggests that directly targeting and inhibiting SRC-3 could impede the growth and spread of pancreatic cancer.

Considering that SRC-3 is involved in multiple growth-signaling pathways, what are the potential implications of inhibiting it as a cancer therapy, and are there any concerns about side effects?

Because SRC-3 influences a wide array of growth-signaling pathways, inhibiting it could have broad effects on cellular processes. While this could be beneficial in slowing cancer growth, there are potential concerns about side effects. For instance, disrupting normal cell functions could lead to unintended consequences. Therefore, precise targeting and careful monitoring would be crucial in any therapeutic approach involving SRC-3 inhibition. Further research is needed to fully understand and mitigate these potential risks.

Given the challenges in treating pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC), how could targeting SRC-3 represent a significant advancement in therapeutic strategies?

Pancreatic cancer, particularly PDAC, is notoriously difficult to treat, with a five-year survival rate of less than 8%. Traditional treatments often fall short, making the need for innovative strategies paramount. Since SRC-3 is overexpressed in PDAC and plays a key role in its growth, migration and invasion, targeting this protein offers a novel approach to disrupt the disease's progression. Successfully inhibiting SRC-3 could lead to more effective, targeted therapies, potentially improving survival rates and the quality of life for patients affected by this devastating illness. This is especially important because traditional treatments have limited success.