Cytokines: Can Cancer Get the Message?

Morris, Rachel; Mortimer, Toni O.; O’Neill, Kim L.

doi:10.3390/cancers14092178

Cited by 38 publications

(20 citation statements)

References 147 publications

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“…We further evaluated the effect of PFPE-CH on the relationship between tumor formation, reactive oxygen species (ROS), and cancer-related cytokines. Cytokines regulate key immune players in cancer development and progression and are potential targets for treatment [84]. In this study, PFPE-CH effectively induced oxidative stress and decreased the levels of IL-4 and IL-6.…”

Section: Pfpe-ch Does Not Cause Chronic Toxicity In Sprague Dawley Ratmentioning

confidence: 59%

Piper nigrum Extract: Dietary Supplement for Reducing Mammary Tumor Incidence and Chemotherapy-Induced Toxicity

Mad-adam,

Madla,

Lailerd

et al. 2023

Foods

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A low piperine fractional Piper nigrum extract (PFPE) was prepared by mixing cold-pressed coconut oil and honey in distilled water, namely, PFPE-CH. In this study, PFPE-CH was orally administered as a dietary supplement to decrease the risk of tumor formation and reduce the side effects of chemotherapeutic drugs during breast cancer treatment. The toxicity study demonstrated no mortality or adverse effects after administrating PFPE-CH at 5000 mg/kg during a 14-day observation period. Additionally, PFPE-CH at 86 mg/kg BW/day did not cause any harm to the kidney or liver function of the rats for six months. In a cancer prevention study, treatment with PFPE-CH at 100 mg/kg BW for 101 days induced oxidative stress and increased the immune response by altering the levels of cancer-associated cytokines (IL-4, IL-6, and IFN-g), leading to a reduction in the tumor incidence of up to 71.4% without any adverse effects. In combination with doxorubicin, PFPE-CH did not disrupt the anticancer effects of the drug in rats with mammary tumors. Surprisingly, PFPE-CH reduced chemotherapy-induced toxicity by improving some hematological and biochemical parameters. Therefore, our results suggest that PFPE-CH is safe and effective in reducing breast tumor incidence and toxicity of chemotherapeutic drugs during cancer treatment in mammary tumor rats.

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Section: Pfpe-ch Does Not Cause Chronic Toxicity In Sprague Dawley Ratmentioning

confidence: 59%

Piper nigrum Extract: Dietary Supplement for Reducing Mammary Tumor Incidence and Chemotherapy-Induced Toxicity

Mad-adam,

Madla,

Lailerd

et al. 2023

Foods

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“…Specifically, nicotine also stimulates cancer growth which are both mediated by the α7 nicotinic-acetylcholine receptors (α7nAChR), possibly involving EGFR. 15,[16][17][18][19] Nicotine stimulates the migration, growth of NSCLC cancer cell lines. 20 A low concentration (1.0 µM) of nicotine has been reported to cause CDDP resistance (Figures 1 and 2).…”

Section: Discussionmentioning

confidence: 99%

“…CDDP's ability to crosslink with the purine bases on DNA has been connected to cell cycle arrest in the G2/M phase‐induced cancer cell apoptosis. Specifically, nicotine also stimulates cancer growth which are both mediated by the α7 nicotinic‐acetylcholine receptors (α7nAChR), possibly involving EGFR 15,16‐19 . Nicotine stimulates the migration, growth of NSCLC cancer cell lines 20 .…”

Section: Discussionmentioning

confidence: 99%

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Rao,

Guo,

2024

Cell Biochemistry & Function

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The majority of adenocarcinoma lung cancer is found in nonsmokers. A history of tobacco use is more common in squamous cell carcinoma of the lung. The aim of this study is to identify the cisplatin (CDDP)‐resistance that promotes lung squamous carcinoma cell growth through nicotine‐mediated HDAC1/7nAchR/E2F/pRb cell cycle activation. Squamous cell carcinoma (NCI‐H520 and NCI‐H157) cells were examined after cisplatin and nicotine treatment by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H‐tetrazolium bromide assay, cell migration assay, immunofluorescence staining, western blot analysis, and immunoprecipitation analysis. Consequently, CDDP is released from DNA and Rb phosphorylated pRb as a result of nicotine‐induced cancer cell proliferation through 7nAchR, which then triggers the opening of the HDAC1 cell cycle. The cell cycle is stopped when CDDP adducts are present. Nicotine exerts cancer cytoprotective effects by allowing HDAC1 repair mechanisms to re‐establish E2F promoting DNA stimulation cell cycle integrity in the cytosol and preventing potential CDDP and HDAC1 suppressed in the nuclear. Concentration expression of nicotine causes squamous carcinoma cell carcinogens to emerge from inflammation. COX2, NF‐KB, and NOS2 increase as a result of nicotine‐induced squamous carcinoma cell inflammation. Nicotine enhanced the cell growth‐related proteins such as α7nAchR, EGFR, HDAC1, Cyclin D, Cyclin E, E2F, Rb, and pRb by western blot analysis. It also induced cancer cell inflammation and growth. As a result, we suggest that nicotine will increase the therapeutic resistance effects of CDDP. This has the potential to interact with nicotine through α7nAchR receptors and HDAC1/Cyclin D/E2F/pRb potentially resulting in CDDP therapy resistance, as well as cell cycle‐induced cancer cell growth.

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“…Alongside cellular and ECM constituents, a diverse range of signaling molecules, such as growth factors, cytokines, and chemokines, are present in the TME [29,30]. These molecules impact cancer cell behavior and immune cell activity and can be secreted by both cancer and stromal cells [31,32].…”

Section: Cd47 Function In the Tme And Signaling Pathwaysmentioning

confidence: 99%

Opportunities and challenges of CD47-targeted therapy in cancer immunotherapy

CHEN,

GUO,

2024

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Cancer immunotherapy has emerged as a promising strategy for the treatment of cancer, with the tumor microenvironment (TME) playing a pivotal role in modulating the immune response. CD47, a cell surface protein, has been identified as a crucial regulator of the TME and a potential therapeutic target for cancer therapy. However, the precise functions and implications of CD47 in the TME during immunotherapy for cancer patients remain incompletely understood. This comprehensive review aims to provide an overview of CD47's multifaced role in TME regulation and immune evasion, elucidating its impact on various types of immunotherapy outcomes, including checkpoint inhibitors and CAR T-cell therapy. Notably, CD47-targeted therapies offer a promising avenue for improving cancer treatment outcomes, especially when combined with other immunotherapeutic approaches. The review also discusses current and potential CD47-targeted therapies being explored for cancer treatment and delves into the associated challenges and opportunities inherent in targeting CD47. Despite the demonstrated effectiveness of CD47-targeted therapies, there are potential problems, including unintended effects on healthy cells, hematological toxicities, and the development if resistance. Consequently, further research efforts are warranted to fully understand the underlying mechanisms of resistance and to optimize CD47-targeted therapies through innovative combination approaches, ultimately improving cancer treatment outcomes. Overall, this comprehensive review highlights the significance of CD47 as a promising target for cancer immunotherapy and provides valuable insight into the challenges and opportunities in developing effective CD47-targeted therapies for cancer treatment.

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Cytokines: Can Cancer Get the Message?

Cited by 38 publications

References 147 publications

Piper nigrum Extract: Dietary Supplement for Reducing Mammary Tumor Incidence and Chemotherapy-Induced Toxicity

Piper nigrum Extract: Dietary Supplement for Reducing Mammary Tumor Incidence and Chemotherapy-Induced Toxicity

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Opportunities and challenges of CD47-targeted therapy in cancer immunotherapy

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