Commitment of Scaffold Proteins in the Onco-Biology of Human Colorectal Cancer and Liver Metastases after Oxaliplatin-Based Chemotherapy

Rotoli, Deborah; Morales, Manuel; Ávila, Julio; Maeso, María del Carmen; García, Maria del Pino; Mobasheri, Ali; Martín‐Vasallo, Pablo

doi:10.3390/ijms18040891

Cited by 16 publications

(19 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Important biological mechanisms may remodel the abundance and activity of modulatory protein hubs: Superenhancers alter both the abundance and the functions and structures at the level of protein production, and scaffold proteins act at the level of protein localization addressing their activity (45)(46)(47). Cytokines, such as interleukin-6 or TGFβ, can switch their function during tumor progression from a growth inhibitor to a growth stimulator (45,48).…”

Section: Communication Unifies All Systems Levelsmentioning

confidence: 99%

Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

et al. 2019

View full text Add to dashboard Cite

The current approach to systemic therapy for metastatic cancer is aimed predominantly at inducing apoptosis of cancer cells by blocking tumor-promoting signaling pathways or by eradicating cell compartments within the tumor. In contrast, a systems view of therapy primarily considers the communication protocols that exist at multiple levels within the tumor complex, and the role of key regulators of such systems. Such regulators may have far-reaching influence on tumor response to therapy and therefore patient survival. This implies that neoplasia may be considered as a cell non-autonomous disease. The multi-scale activity ranges from intra-tumor cell compartments, to the tumor, to the tumor-harboring organ to the organism. In contrast to molecularly targeted therapies, a systems approach that identifies the complex communications networks driving tumor growth offers the prospect of disrupting or "normalizing" such aberrant communicative behaviors and therefore attenuating tumor growth. Communicative reprogramming, a treatment strategy referred to as anakoinosis, requires novel therapeutic instruments, so-called master modifiers to deliver concerted tumor growth-attenuating action. The diversity of biological outcomes following pro-anakoinotic tumor therapy, such as differentiation, trans-differentiation, control of tumor-associated inflammation, etc. demonstrates that long-term tumor control may occur in multiple forms, inducing even continuous complete remission. Accordingly, pro-anakoinotic therapies dramatically extend the repertoire for achieving tumor control and may activate apoptosis pathways for controlling resistant metastatic tumor disease and hematologic neoplasia.

show abstract

Section: Communication Unifies All Systems Levelsmentioning

confidence: 99%

Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Likewise, high tumor PGE2 expression represents a key mediator of immune resistance, mainly due to the secretion of suppressive chemokines and the recruitment of MDSCs, which results in immunogenic loss. [120,121]. Regulatory T cells (Tregs) are a heterogeneous subpopulation of T lymphocytes, which play a crucial role in tolerance maintaining [122].…”

Section: Regulation Of the Antitumor T-cell Immunitymentioning

confidence: 99%

Strategy to targeting the immune resistance and novel therapy in colorectal cancer

Wang

Guan

et al. 2018

Cancer Medicine

View full text Add to dashboard Cite

Assessing the CRC subtypes that can predict the outcome of colorectal cancer (CRC) in patients with immunogenicity seems to be a promising strategy to develop new drugs that target the antitumoral immune response. In particular, the disinhibition of the antitumoral T‐cell response by immune checkpoint blockade has shown remarkable therapeutic promise for patients with mismatch repair (MMR) deficient CRC. In this review, the authors provide the update of the molecular features and immunogenicity of CRC, discuss the role of possible predictive biomarkers, illustrate the modern immunotherapeutic approaches, and introduce the most relevant ongoing preclinical study and clinical trials such as the use of the combination therapy with immunotherapy. Furthermore, this work is further to understand the complex interactions between the immune surveillance and develop resistance in tumor cells. As expected, if the promise of these developments is fulfilled, it could develop the effective therapeutic strategies and novel combinations to overcome immune resistance and enhance effector responses, which guide clinicians toward a more “personalized” treatment for advanced CRC patients.

show abstract

“…Accumulating data have demonstrated that FKBP51 serves important functions in tumor cell growth, apoptosis, and sensitivity to radiotherapy and chemotherapy ( 30 , 31 ). Studies have demonstrated that FKBP51 may serve a positive function in tumor progression by activating the NF-κB ( 32 – 34 ) pathway, or a negative function by promoting the Akt pathway through the dephosphorylation of Akt Ser473 to inhibit cell proliferation ( 9 , 35 ).…”

Section: Discussionmentioning

confidence: 99%

FKBP51 promotes migration and invasion of papillary thyroid carcinoma through NF‑κB‑dependent epithelial‑to‑mesenchymal transition

et al. 2018

View full text Add to dashboard Cite

FK506-binding protein 51 (FKBP51) is a member of the immunophilin family, with relevant roles in multiple signaling pathways, tumorigenesis and chemoresistance. However, the function of FKBP51 in papillary thyroid carcinoma (PTC) remains largely unknown. In the present study, increased FKBP51 expression was detected in PTC tissues as compared with adjacent normal tissues, and the expression level was associated with clinical tumor, node and metastasis stage. Using FKBP51-overexpressing K1 cells and FKBP51-knockdown TPC-1 cells, both human PTC cell lines, it was identified that FKBP51 promoted the migration and invasion of PTC, without affecting cell proliferation. Further investigation revealed that FKBP51 activated the NF-κB pathway and epithelial-to-mesenchymal transition (EMT) genes, and EMT was suppressed when NF-κB was inhibited. It was also assessed whether FKBP51 promoted the formation of cytoskeleton to promote migration and invasion of PTC using a tubulin tracker; however, no evidence of such an effect was observed. These results suggested that FKBP51 promotes migration and invasion through NF-κB-dependent EMT.

show abstract

Commitment of Scaffold Proteins in the Onco-Biology of Human Colorectal Cancer and Liver Metastases after Oxaliplatin-Based Chemotherapy

Cited by 16 publications

References 65 publications

Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

Anakoinosis: Correcting Aberrant Homeostasis of Cancer Tissue—Going Beyond Apoptosis Induction

Strategy to targeting the immune resistance and novel therapy in colorectal cancer

FKBP51 promotes migration and invasion of papillary thyroid carcinoma through NF‑κB‑dependent epithelial‑to‑mesenchymal transition

Contact Info

Product

Resources

About