Camel Milk and Tumour Management: Exploring Immunomodulatory & Anti-Proliferative Effects

Cancer remains a leading cause of global mortality, with conventional therapies often limited by toxicity, resistance, and immunosuppression. This has spurred scientific interest in natural adjuvants that may complement standard treatments. Camel milk (CM), a traditional therapeutic in arid regions, has emerged as a compelling candidate for oncology research due to its unique biochemical composition. Contemporary studies reveal that CM is not merely a nutritional source but a complex biological fluid rich in bioactive molecules with targeted anti-neoplastic properties. This review synthesizes current evidence on CM’s potential role in tumour management, focusing on its anti-proliferative and immunomodulatory mechanisms, while contextualizing its realistic application as a supportive agent in cancer care.

The therapeutic potential of CM stems from its diverse array of bioactive compounds, many absent or present in lower concentrations in bovine milk. Lactoferrin, a multifunctional iron-binding glycoprotein, constitutes a significant component, demonstrating direct anti-cancer actions, including induction of apoptosis and inhibition of angiogenesis. Immunoglobulins (IgG, secretory IgA) in CM exhibit higher relative abundance, contributing to pathogen neutralization and potential anti-tumour immunity. Furthermore, CM contains lysozyme, lactoperoxidase, and alpha-lactalbumin, each contributing to its bioactivity. Notably, CM-derived exosomes (CM-EXOs)—nanoscale vesicles (40–150 nm) carrying proteins, lipids, and regulatory RNAs—have garnered attention for their role in intercellular communication and their stability against gastrointestinal degradation, facilitating bioactive delivery. Upon digestion, milk proteins release bioactive peptides with documented anti-proliferative, antioxidant, and immunomodulatory sequences.

Table 1: Key Bioactive Components in Camel Milk with Anti-Cancer Potential

A cornerstone of CM’s anti-cancer potential lies in its ability to directly inhibit tumour cell proliferation and viability. Numerous in vitro studies demonstrate CM’s cytotoxic effects across various cancer cell lines. For instance, CM significantly reduced proliferation and viability in human breast cancer (MCF-7) and colorectal cancer (HCT-116) cells. Mechanistic studies revealed this involved the induction of autophagy—a cellular self-degradation process—characterized by increased LC3-II protein accumulation, decreased p62 expression, and the formation of autophagosomes. Beyond whole milk, specific bioactive components exhibit potent activity. Lactoferrin-derived peptides, particularly PEP66 (identified via in silico design and in vitro validation), showed remarkable anti-proliferative effects against MCF-7 cells (IC50 = 52.82 μg/mL). Molecular docking and dynamics simulations demonstrated PEP66’s stable interaction with key residues in the HER2 catalytic site, a critical driver in many breast cancers, suggesting a targeted molecular mechanism. Furthermore, CM-EXOs exert selective cytotoxicity. They induce apoptosis in liver (HepG2) and colon (CaCo2) cancer cells, evidenced by elevated Bax (pro-apoptotic), caspase-3 activation, and reduced Bcl-2 (anti-apoptotic) expression, while sparing normal Vero cells. CM-EXOs also elevate intracellular reactive oxygen species (ROS) specifically in cancer cells, exploiting their often-compromised antioxidant defences. Animal models corroborate these findings. Local injection or oral administration of CM-EXOs in MCF-7 tumour-bearing rats significantly reduced tumour volume, associated with increased apoptosis markers (DNA fragmentation, caspase-3) and downregulated metastasis (MMP-9, ICAM-1) and angiogenesis (VEGF) genes. These studies illustrate CM’s multi-pronged anti-proliferative approach, targeting fundamental cancer hallmarks like sustained proliferation, evasion of cell death, and metastasis.

Beyond direct tumour cell killing, CM exerts significant immunomodulatory effects, potentially enhancing the body’s innate and adaptive defences against cancer. Chronic inflammation and immune dysfunction are hallmarks of cancer progression. CM components modulate immune cell activity and cytokine profiles. Studies show CM consumption increases spleen CD4+, CD8+ T cells, and NK1.1+ natural killer cells in tumour-bearing animals, indicating enhanced systemic immune response and potential for improved immune surveillance. Bioactive peptides derived from fermented CM, prevalent in traditional diets like those of the Kazakh population in Xinjiang, demonstrate immunoregulatory potential. Network pharmacology and molecular docking studies predict these peptides modulate targets involved in immune signalling pathways (e.g., pathways in cancer, lipid and atherosclerosis signalling), influencing the expression of cytokines like IFN-γ, which is crucial for anti-tumour immunity. Furthermore, CM possesses potent anti-inflammatory properties. It reduces the expression of pro-inflammatory cytokines (IL-1β, TNF-α) and transcription factors (NF-κB) within the tumour microenvironment in vivo. This attenuation of chronic inflammation is significant, as inflammatory mediators promote tumour growth, angiogenesis, and immunosuppression. The immunoglobulins and lactoferrin in CM also contribute to its immune-balancing effects, potentially aiding in restoring immune homeostasis disrupted by cancer or conventional cytotoxic therapies like chemotherapy. This immunomodulation, shifting the balance towards a more robust anti-tumour immune response while dampening tumour-promoting inflammation, represents a valuable supportive mechanism in oncology.

Oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defence mechanisms, plays a crucial role in carcinogenesis, DNA damage, and cancer therapy-related toxicity. CM is a rich source of diverse antioxidants functioning synergistically. It contains notably high levels of vitamin C (3-5 times more than cow milk), which acts as a potent free radical scavenger. Furthermore, proteins like alpha-lactalbumin and beta-casein, and their enzymatically hydrolysed peptides, exhibit significant antioxidant activity by reducing ROS, hydroxyl radicals, nitric oxide (NO), superoxide anions, and peroxyl radicals. Lactoferrin contributes through iron chelation, preventing iron-catalysed ROS generation via the Fenton reaction. CM administration in tumour-bearing models consistently demonstrates the restoration of antioxidant status. It increases the activities of key endogenous antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) within tumour tissue and systemically, while simultaneously decreasing lipid peroxidation markers like malondialdehyde (MDA) and downregulating pro-oxidative enzymes such as inducible nitric oxide synthase (iNOS) 7810. CM-EXOs contribute uniquely by downregulating the expression of antioxidant-related genes (Nrf2, HO-1) specifically in cancer cells, thereby increasing their vulnerability to oxidative damage, while bolstering antioxidant defences in normal tissues. This dual action—enhancing systemic antioxidant capacity to mitigate therapy side effects and potentially exacerbating oxidative stress selectively within cancer cells—highlights CM’s multifaceted role in managing oxidative stress associated with cancer.

The accumulated evidence positions camel milk, particularly its bioactive components, as a potential adjunctive therapy in comprehensive tumour management rather than a standalone cure. Its value lies in several supportive roles: potentially inhibiting tumour growth through direct anti-proliferative and pro-apoptotic effects; mitigating the immunosuppressive effects of chemotherapy and radiotherapy by enhancing immune cell populations and function; providing high-quality protein, essential vitamins (especially C, A, E, B complex), and minerals (Zinc, Selenium) to combat cancer-associated malnutrition and cachexia; and reducing oxidative stress and inflammation systemically, potentially improving patient tolerance to treatments and quality of life. However, significant challenges remain. Most evidence derives from in vitro studies and animal models; rigorously designed human clinical trials are scarce and urgently needed to establish efficacy, optimal dosing (whole milk vs. isolates like exosomes or lactoferrin peptides), bioavailability, and safety profiles, especially during active cancer treatments. The variability in CM composition based on geography, breed, diet, and lactation stage necessitates standardization for therapeutic applications.

Future research should focus on elucidating precise molecular mechanisms of key bio actives (e.g., exosomal miRNAs, specific peptide sequences), developing efficient delivery systems (e.g., encapsulating exosomes or peptides for enhanced stability and targeting), and exploring synergistic effects with conventional chemo- or immunotherapies. While camel milk presents a promising natural adjuvant in oncology, its integration into clinical practice demands robust scientific validation through human studies and careful consideration within evidence-based cancer care frameworks.

Glossary

1. Adjuvant Therapy: Treatment given in addition to the primary (main) therapy to enhance its effectiveness or manage side effects (e.g., using camel milk alongside chemotherapy).
2. Angiogenesis: The formation of new blood vessels; tumours promote angiogenesis to supply oxygen and nutrients for growth. CM components (e.g., lactoferrin) can inhibit this process.
3. Apoptosis: A form of programmed, controlled cell death. Induction of apoptosis in cancer cells is a key anti-cancer mechanism of CM components like lactoferrin peptides and exosomes.
4. Autophagy: A cellular “clean-up” process where cells break down and recycle their own components. CM can induce autophagy, leading to cancer cell death.
5. Bioactive Peptides: Short sequences of amino acids released from proteins (e.g., during digestion or fermentation) that exert specific biological effects, such as anti-cancer or immunomodulatory activities.
6. Exosomes (CM-EXO): Small extracellular vesicles (40-150 nm) naturally released by cells, found abundantly in camel milk. They transport bioactive molecules (proteins, RNAs) and can influence recipient cell behaviour, including inducing selective cancer cell death.
7. Immunomodulation: The process of modifying or regulating the immune system’s responses. CM can enhance anti-tumour immune responses (e.g., boosting T cells, NK cells) while suppressing harmful inflammation.
8. Lactoferrin: An iron-binding glycoprotein found in high concentrations in camel milk. It exhibits multiple anti-cancer properties including direct cytotoxicity, immune modulation, iron chelation, and anti-angiogenic effects.
9. Oxidative Stress: An imbalance between the production of harmful reactive oxygen species (ROS) and the body’s ability to detoxify them. Chronic oxidative stress contributes to cancer development and progression. CM acts as a potent antioxidant.
10. Selective Cytotoxicity: The ability of an agent to kill specific cells (e.g., cancer cells) while causing minimal damage to normal cells. CM exosomes demonstrate this property.

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