Illustration of TCCP molecules inducing apoptosis in a cancer cell.

Triple-Negative Breast Cancer: Can a Natural Compound Hold the Key to New Treatments?

Soraya Malik in Health & Wellness August 2025 • 4 min read.

"Research explores how a pyrrole-based molecule from Tinospora cordifolia could revolutionize TNBC therapy by targeting cancer cells' weaknesses."

Triple-negative breast cancer (TNBC) accounts for approximately 15% of all breast cancer diagnoses worldwide, posing a significant challenge due to its aggressive nature and lack of targeted therapies. Unlike other breast cancer subtypes that express estrogen, progesterone, or HER2 receptors, TNBC lacks these markers, rendering traditional hormone therapies ineffective. This absence of specific targets makes TNBC difficult to treat and often results in poorer outcomes for patients.

The urgent need for innovative treatments has driven researchers to explore alternative approaches, including the investigation of natural compounds with anti-cancer properties. One promising avenue involves the medicinal plant Tinospora cordifolia, known for its diverse array of bioactive molecules, including alkaloids, steroids, and glycosides. These compounds have demonstrated various therapeutic effects, including anti-neoplastic, anti-metastatic, and anti-angiogenic activities.

Recent research has focused on a pyrrole-based small molecule, Bis(2-ethyl hexyl) 1H-pyrrole-3,4-dicarboxylate (TCCP), derived from Tinospora cordifolia. This molecule has shown potential in suppressing heat shock response and tumor angiogenesis. New studies suggest that TCCP can induce apoptosis—programmed cell death—in TNBC cells, offering a novel strategy to combat this challenging cancer. Let’s dive into the science behind TCCP and its potential impact on TNBC treatment.

How Does TCCP Target and Destroy TNBC Cells?

Illustration of TCCP molecules inducing apoptosis in a cancer cell.

The study published in Chemico-Biological Interactions (2019) explores TCCP's mechanism of action in inducing apoptosis in MDA-MB-231 cells, a common TNBC cell line. Researchers examined various apoptotic markers to understand how TCCP triggers cell death. The key processes include:

Here's a breakdown of how TCCP works:

ROS Generation: TCCP increases the production of reactive oxygen species (ROS) within the cancer cells. High levels of ROS cause oxidative stress, damaging cellular components and triggering apoptosis.
Calcium Increase: TCCP elevates intracellular calcium levels, disrupting normal cell signaling and contributing to mitochondrial dysfunction.
Mitochondrial Damage: TCCP disrupts the mitochondrial membrane potential (ΔΨm), leading to mitochondrial permeability transition pore (MPTP) opening and cardiolipin peroxidation. These events compromise mitochondrial function and trigger the release of cytochrome c.
Caspase Activation: Cytochrome c release activates caspases, a family of proteases that execute the apoptotic program. Caspase activation leads to DNA fragmentation and cell death.
p53 Restoration: TCCP restores the activity of the p53 protein, a tumor suppressor that is often inactive or mutated in cancer cells. Activated p53 promotes apoptosis and inhibits tumor growth.

In essence, TCCP targets multiple pathways within TNBC cells, overwhelming their defenses and inducing programmed cell death. This multi-faceted approach makes TCCP a promising candidate for further development as a TNBC therapy.

The Future of TCCP in Cancer Treatment

While these findings are promising, it’s important to remember that this research is still in its early stages. More studies are needed to fully understand TCCP’s effects, optimize its use, and evaluate its safety in humans. However, the potential of TCCP to target TNBC through multiple mechanisms offers a new avenue for developing effective and less toxic treatments. As research progresses, TCCP and similar natural compounds could play a significant role in improving outcomes for individuals facing this challenging disease.

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: 10.1016/j.cbi.2018.12.005, Alternate LINK

Title: A New Pyrrole Based Small Molecule From Tinospora Cordifolia Induces Apoptosis In Mda-Mb-231 Breast Cancer Cells Via Ros Mediated Mitochondrial Damage And Restoration Of P53 Activity

Subject: Toxicology

Journal: Chemico-Biological Interactions

Publisher: Elsevier BV

Authors: K.C. Rashmi, M. Harsha Raj, Manoj Paul, Kesturu S. Girish, Bharathi P. Salimath, H.S. Aparna

Published: 2019-02-01

Everything You Need To Know

What is Triple-Negative Breast Cancer (TNBC), and why is it so difficult to treat?

Triple-Negative Breast Cancer (TNBC) is a specific subtype of breast cancer, accounting for about 15% of all diagnoses globally. It's termed 'triple-negative' because it lacks the estrogen, progesterone, and HER2 receptors that are typically targeted by hormone therapies in other breast cancer subtypes. This absence of specific targets makes TNBC particularly challenging to treat with conventional methods, often resulting in poorer patient outcomes due to the aggressive nature of the cancer cells and the lack of effective targeted therapies. This necessitates the exploration of alternative treatment strategies like those involving natural compounds.

How does the natural compound TCCP derived from Tinospora cordifolia, work against TNBC?

TCCP, a pyrrole-based molecule extracted from the medicinal plant Tinospora cordifolia, targets multiple pathways in TNBC cells to induce apoptosis, or programmed cell death. It works through several mechanisms: It increases the production of reactive oxygen species (ROS), causing oxidative stress; elevates intracellular calcium levels, disrupting cell signaling; damages mitochondria, leading to the release of cytochrome c; activates caspases, which execute the apoptotic program; and restores the activity of the p53 protein, a tumor suppressor. These combined effects overwhelm the cancer cells, leading to their destruction.

What are the key processes involved in TCCP's mechanism of action against TNBC cells, as demonstrated in the Chemico-Biological Interactions (2019) study?

The Chemico-Biological Interactions (2019) study outlines several key steps in how TCCP induces apoptosis in MDA-MB-231 cells, a TNBC cell line. First, TCCP increases ROS generation, creating oxidative stress that damages cellular components. Second, it elevates intracellular calcium levels, disrupting normal cell signaling and potentially causing mitochondrial dysfunction. Third, TCCP damages the mitochondrial membrane, leading to the opening of the mitochondrial permeability transition pore (MPTP) and the release of cytochrome c. This cytochrome c release activates caspases, which are proteases that execute apoptosis. Finally, TCCP restores the activity of the p53 protein, promoting apoptosis and inhibiting tumor growth. Together, these processes make TCCP a promising agent for TNBC therapy.

Can you explain the significance of p53 restoration in the context of TCCP's treatment of TNBC?

The restoration of p53 activity is crucial in TCCP's mechanism because p53 is a tumor suppressor protein that is often inactive or mutated in cancer cells, including TNBC cells. When p53 is functional, it plays a critical role in initiating apoptosis and inhibiting tumor growth. TCCP's ability to restore p53 function allows it to re-establish the body's natural defense mechanisms against cancer. This restoration helps trigger programmed cell death in the cancer cells, making them more susceptible to being eliminated. This is a significant advantage, as it addresses a fundamental issue within the cancer cells themselves, leading to more effective and targeted treatment.

What are the next steps for TCCP as a potential TNBC treatment, and what challenges remain?

The research on TCCP is still in its early stages. While initial findings are promising, more studies are needed to fully understand the compound's effects, optimize its use, and evaluate its safety in humans. The next steps include conducting further pre-clinical studies to confirm efficacy and safety, determining the optimal dosage and delivery methods, and understanding any potential side effects. Successfully navigating these challenges will be critical for TCCP to move towards clinical trials and, ultimately, potentially become a new therapeutic option for individuals facing TNBC. Moreover, it is important to monitor any long term effects that may result from using TCCP, which may influence the frequency of its use.