Cancers take their Toll—the function and regulation of Toll-like receptors in cancer cells

Chen, R; Alvero, Ayesha B.; Da, Silasi; Kd, Steffensen; G, Mor

doi:10.1038/sj.onc.1210907

Cited by 183 publications

(151 citation statements)

References 71 publications

(82 reference statements)

Supporting

Mentioning

146

Contrasting

Unclassified

Order By: Relevance

“…The signature of enhanced PRR mRNAs might indicate an antitumorigenic effect of TLRs, NLRs, and RIG-I-like receptors in remitting VX2 tumors, albeit protumorigenic effects of PRRs are also known (34,35).…”

Section: Discussionmentioning

confidence: 99%

Intraperitoneal Oxidative Stress in Rabbits with Papillomavirus-Associated Head and Neck Cancer Induces Tumoricidal Immune Response That Is Adoptively Transferable

Rossmann

Mandic

Heinis

et al. 2014

Clinical Cancer Research

View full text Add to dashboard Cite

Purpose: How tumors evade or suppress immune surveillance is a key question in cancer research, and overcoming immune escape is a major goal for lengthening remission after cancer treatment. Here, we used the papillomavirus-associated rabbit auricular VX2 carcinoma, a model for studying human head and neck cancer, to reveal the mechanisms underlying the antitumorigenic effects of intraperitoneal oxidative stressExperimental Design: Solid auricular VX2 tumors were induced in immune-competent adult New Zealand White Rabbits. Animals were O 3 /O 2 -PP-or sham-treated, after which they underwent tumor ablation upon reaching no-go criteria. CD3 þ tumor-infiltrating lymphocytes (TIL) were evaluated by immunohistochemistry, and expression levels of 84 immune response genes were measured by quantitative real-time PCR. Adoptive transfer of peripheral blood leukocytes (PBL)-derived from animals with tumor regression-into control animals with progressing tumors was implemented to assess acquired tumor resistance functionally. Results: Auricular VX2 tumors regressing after O 3 /O 2 -PP treatment exhibited increased levels of CD3 þ TILs; they also exhibited enhanced expression of genes that encode receptors involved in pattern recognition, molecules that are required for antigen presentation and T cell activation, and inflammatory mediators. Adoptive cell transfer of PBLs from donor rabbits with regressing tumors to recipient rabbits with newly implanted VX2 carcinoma resulted in acquired tumor resistance of the host and tumor regression. Conclusion: Intraperitoneal oxidative stress effectively converts the immune response against the papillomavirus-associated rabbit VX2 carcinoma from tumor permissive to tumoricidal and leads to a sustainable, adoptively transferable oncolytic immune response. Clin Cancer Res; 20(16); 4289-301. Ó2014 AACR.

show abstract

Section: Discussionmentioning

confidence: 99%

Intraperitoneal Oxidative Stress in Rabbits with Papillomavirus-Associated Head and Neck Cancer Induces Tumoricidal Immune Response That Is Adoptively Transferable

Rossmann

Mandic

Heinis

et al. 2014

Clinical Cancer Research

View full text Add to dashboard Cite

show abstract

“…In advanced OC, resistance to chemotherapy is a major factor limiting long-term treatment against OC (Fallows et al 2001), and drug resistance has been recognized to induce pro-tumor activities (Kelly et al 2006, Chen et al 2008.…”

Section: Introductionmentioning

confidence: 99%

Apoptosis is triggered by melatonin in an in vivo model of ovarian carcinoma

Chuffa¹,

Alves²,

Martinez³

et al. 2015

Endocrine-Related Cancer

View full text Add to dashboard Cite

Apoptosis plays an important role in the treatment of cancer, and targeting apoptosis-related molecules in ovarian cancer (OC) is of great therapeutic value. Melatonin (Mel) is an indoleamine displaying several anti-cancer properties and has been reported to modulate apoptosis signaling in multiple tumor subtypes. We investigated OC and the role of Mel therapy on the pro-apoptotic (p53, BAX, caspase-3, and cleaved caspase-3) and anti-apoptotic (Bcl-2 and survivin) proteins in an ethanol (EtOH)-preferring rat model. To induce OC, the left ovary was injected directly with a single dose of 100 mg 7,12-dimethylbenz(a)anthracene dissolved in 10 ml of sesame oil under the bursa. Right ovaries were used as sham-surgery controls. After developing OC, half of the animals received i.p. injections of Mel (200 mg/100 g BW per day) for 60 days. Body weight gain, EtOH consumption, and energy intake were unaffected by the treatments. Interestingly, absolute and relative OC masses showed a significant reduction after Mel therapy, regardless of EtOH consumption. To accomplish OC-related apoptosis, we first observed that p53, BAX, caspase-3, and cleaved caspase-3 were downregulated in OC tissue while Bcl-2 and survivin were overexpressed. Notably, Mel therapy and EtOH intake promoted apoptosis along with the upregulation of p53, BAX, and cleaved caspase-3. Fragmentation of DNA observed by TUNEL-positive nuclei was also enhanced following Mel treatment. In addition, Bcl-2 was downregulated by the EtOH intake and lower survivin levels were observed after Mel therapy. Taken together, these results suggest that Mel induce apoptosis in OC cells of EtOH-preferring animals.Key Words " ovarian cancer " melatonin " pro-apoptotic protein " anti-apoptotic protein

show abstract

“…Autophagy triggered by TLR3 and TLR4 was shown to contribute to the progression of lung cancer [12]. However, several studies have suggested that TLR activation enhances the survival, proliferation, and metastasis of cancer cells [12,16,17,18,19]. Furthermore, TLRs trigger the release of proinflammatory cytokines, chemokines, and immunosuppressive factors, leading to immune evasion and enhanced cancer cell resistance [12,19].…”

Section: Autophagy As An Innate Immune Response Against Cancermentioning

confidence: 99%

Molecular interactions of autophagy with the immune system and cancer

Hong¹,

Jin²,

Hong³

et al. 2017

Preprint

View full text Add to dashboard Cite

Autophagy is a highly conserved catabolic mechanism that mediates the degradation of damaged cellular components by inducing their fusion with lysosomes. This process provides cells with an alternative source of energy for the synthesis of new proteins and the maintenance of metabolic homeostasis in stressful environments. Numerous studies have demonstrated beneficial roles for the induction as well as the suppression of autophagy in cancer cells. Autophagy may induce either survival or death depending on the cell/tissue type. Radiation therapy is widely used therapeutic option to treat cancer, and it induces autophagy in human cancer cell line. Also, melatonin seems to affect cancer cell death via regulation of programmed cell death. In this review, we summarize the current understanding of autophagy and its regulation in cancer.

show abstract

Cancers take their Toll—the function and regulation of Toll-like receptors in cancer cells

Cited by 183 publications

References 71 publications

Intraperitoneal Oxidative Stress in Rabbits with Papillomavirus-Associated Head and Neck Cancer Induces Tumoricidal Immune Response That Is Adoptively Transferable

Intraperitoneal Oxidative Stress in Rabbits with Papillomavirus-Associated Head and Neck Cancer Induces Tumoricidal Immune Response That Is Adoptively Transferable

Apoptosis is triggered by melatonin in an in vivo model of ovarian carcinoma

Molecular interactions of autophagy with the immune system and cancer

Contact Info

Product

Resources

About