Thiazolidinediones abrogate cervical cancer growth

Wuertz, Beverly R.; Darrah, Lindsay; Wudel, Justin; Ondrey, Frank G.

doi:10.1016/j.yexcr.2017.02.020

Cited by 11 publications

(12 citation statements)

References 48 publications

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“…These findings extend additional published findings in head and neck cancer and cervical carcinoma cell lines we have recently published with other thiazolidinediones and PPARγ activators. 51,52 They also augment other findings we have recently published in lung carcinogenesis animal models. 53,54 The capacity for this agent to affect cells that have undergone initiation and promotion in vivo (lung) or are overtly cancerous (squamous carcinoma cell lines, both human papillomavirus positive and negative) provides the rationale for their use in the preneoplastic cell lines examined herein.…”

Section: Introductionsupporting

confidence: 84%

PPARγ-Mediated p21 Induction in Aerodigestive Preneoplastic Cell Lines

Miller

Wuertz

Ondrey

2018

Ann Otol Rhinol Laryngol

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Section: Introductionsupporting

confidence: 84%

PPARγ-Mediated p21 Induction in Aerodigestive Preneoplastic Cell Lines

Miller

Wuertz

Ondrey

2018

Ann Otol Rhinol Laryngol

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“…Cervical cancer is a serious malignancy in women worldwide. 31,33 Cancer can weaken the role of the autoimmune system, and the common methods for cancer treatment are radiation therapy, chemotherapy, surgery, or a combination of these. 34−36 If cervical cancer is caught and treated early, whether with surgery or radiation therapy, it is highly curable, but if found in the middle or late stages, treatment efficacy is poor.…”

Section: Discussionmentioning

confidence: 99%

Cervical Cancer HeLa Cell Autocrine Apoptosis Induced by Coimmobilized IFN-γ plus TNF-α Biomaterials

Zhang

Chen

et al. 2018

ACS Appl. Mater. Interfaces

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Using external methods to induce the death of cancer cells is recognized as one of the main strategies for cancer treatment. Research indicated that TNF-α is frequently used in tumor biotherapy while IFN-γ can directly inhibit tumor cell proliferation. In our study, TNF-α and IFN-γ were coimmobilized on polystyrene material (PSt) or FeO-oleic acid nanoparticles (NPs). Then the structural change of these two proteins can be observed. Meanwhile, the expressions of both TNF-α and IFN-α increased significantly, as determined by gene microarray analysis; however, in the presence of TNF-α plus IFN-α inhibitors, TNF-α and IFN-α did not increase in HeLa cells induced by coimmobilized IFN-γ plus TNF-α. Our results indicate that such change can stimilate HeLa cells to secrete more TNF-α and IFN-α, by which the apoptosis of HeLa cells could be further induced. This study is the first report of autocrine-induced apoptosis of HeLa cells. In addition, we performed ELISA, RT-PCR, flow cytometry, and Western blot analyses, as well as a series of analytical tests at the animal level. our data also indicate that the PSt-coimmobilized IFN-γ plus TNF-α has apparent effects for cancer treatment in vivo, which is of great significance for translation into clinical medicine.

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“…While this might be mediated by the antidiabetic effects of TZDs, there is also evidence for TZDs directly inhibiting growth of established tumors. Moreover, TZDs are in fact discussed for cancer therapy (154,155). One concern using TZDs is, however, the notion that PPAR-g also plays an important role in Tregs as Treg accumulation in adipose tissue has been shown to be PPAR-gdependent (156).…”

Section: Interactions Of Th2 Cell Metabolism Tme and Potential Therapeutic Strategiesmentioning

confidence: 99%

Metabolic Interdependency of Th2 Cell-Mediated Type 2 Immunity and the Tumor Microenvironment

et al. 2021

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The function of T cells is critically dependent on their ability to generate metabolic building blocks to fulfil energy demands for proliferation and consecutive differentiation into various T helper (Th) cells. Th cells then have to adapt their metabolism to specific microenvironments within different organs during physiological and pathological immune responses. In this context, Th2 cells mediate immunity to parasites and are involved in the pathogenesis of allergic diseases including asthma, while CD8+ T cells and Th1 cells mediate immunity to viruses and tumors. Importantly, recent studies have investigated the metabolism of Th2 cells in more detail, while others have studied the influence of Th2 cell-mediated type 2 immunity on the tumor microenvironment (TME) and on tumor progression. We here review recent findings on the metabolism of Th2 cells and discuss how Th2 cells contribute to antitumor immunity. Combining the evidence from both types of studies, we provide here for the first time a perspective on how the energy metabolism of Th2 cells and the TME interact. Finally, we elaborate how a more detailed understanding of the unique metabolic interdependency between Th2 cells and the TME could reveal novel avenues for the development of immunotherapies in treating cancer.

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Thiazolidinediones abrogate cervical cancer growth

Cited by 11 publications

References 48 publications

PPARγ-Mediated p21 Induction in Aerodigestive Preneoplastic Cell Lines

PPARγ-Mediated p21 Induction in Aerodigestive Preneoplastic Cell Lines

Cervical Cancer HeLa Cell Autocrine Apoptosis Induced by Coimmobilized IFN-γ plus TNF-α Biomaterials

Metabolic Interdependency of Th2 Cell-Mediated Type 2 Immunity and the Tumor Microenvironment

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