Type III Interferons IL-28 and IL-29: Novel Interferon Family Members with Therapeutic Potential in Cancer Therapy

Classic and Novel Signaling Pathways Involved in Cancer: Targeting the NF-κB and Syk Signaling Pathways

Current Stem Cell Research & Therapy ◽

10.2174/1574888x13666180723104340 ◽

2019 ◽

Vol 14 (3) ◽

pp. 219-225 ◽

Cited By ~ 6

Author(s):

Cong Tang ◽

Guodong Zhu

Keyword(s):

Cancer Therapy ◽

Tyrosine Kinase ◽

Signaling Pathways ◽

Molecular Mechanisms ◽

Therapeutic Potential ◽

Cell Receptor ◽

Transmembrane Receptors ◽

Biological Responses ◽

Different Types

The nuclear factor kappa B (NF-κB) consists of a family of transcription factors involved in the regulation of a wide variety of biological responses. Growing evidence support that NF-κB plays a major role in oncogenesis as well as its well-known function in the regulation of immune responses and inflammation. Therefore, we made a review of the diverse molecular mechanisms by which the NF-κB pathway is constitutively activated in different types of human cancers and the potential role of various oncogenic genes regulated by this transcription factor in cancer development and progression. We also discussed various pharmacological approaches employed to target the deregulated NF-κB signaling pathway and their possible therapeutic potential in cancer therapy. Moreover, Syk (Spleen tyrosine kinase), non-receptor tyrosine kinase which mediates signal transduction downstream of a variety of transmembrane receptors including classical immune-receptors like the B-cell receptor (BCR), which can also activate the inflammasome and NF-κB-mediated transcription of chemokines and cytokines in the presence of pathogens would be discussed as well. The highlight of this review article is to summarize the classic and novel signaling pathways involved in NF-κB and Syk signaling and then raise some possibilities for cancer therapy.

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Assessment of the therapeutic potential of hesperidin and proteomic resolution of diabetes-mediated neuronal fluctuations expediting Alzheimer’s disease

RSC Advances ◽

10.1039/c5ra01977j ◽

2015 ◽

Vol 5 (58) ◽

pp. 46965-46980 ◽

Cited By ~ 7

Author(s):

Sapna Khowal ◽

Malik M. A. Mustufa ◽

Naveen K. Chaudhary ◽

Samar Husain Naqvi ◽

Suhel Parvez ◽

...

Keyword(s):

Diabetes Mellitus ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Therapeutic Potential ◽

Neuronal Damage ◽

Early Stage ◽

Type Iii

Alzheimer’s disease (AD) has been proposed as type III diabetes mellitus. Prognosis and early stage diagnosis of AD is essentially required in diabetes to avoid extensive irreversible neuronal damage.

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Therapeutic potential of CAR-T cell-derived exosomes: a cell-free modality for targeted cancer therapy

Oncotarget ◽

10.18632/oncotarget.6175 ◽

2015 ◽

Vol 6 (42) ◽

pp. 44179-44190 ◽

Cited By ~ 44

Author(s):

Xiang-Jun Tang ◽

Xu-Yong Sun ◽

Kuan-Ming Huang ◽

Li Zhang ◽

Zhuo-Shun Yang ◽

...

Keyword(s):

T Cell ◽

Cancer Therapy ◽

Therapeutic Potential ◽

Targeted Cancer Therapy ◽

Car T Cell ◽

Car T ◽

A Cell

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Therapeutic potential of intrabodies in cancer therapy

Journal of Clinical & Cellular Immunology ◽

10.4172/2155-9899-c2-050 ◽

2018 ◽

Vol 09 ◽

Author(s):

Thomas Boldicke

Keyword(s):

Cancer Therapy ◽

Therapeutic Potential

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Therapeutic Potential of LNP-Mediated Delivery of miR-634 for Cancer Therapy

Molecular Therapy — Nucleic Acids ◽

10.1016/j.omtn.2019.10.045 ◽

2020 ◽

Vol 19 ◽

pp. 330-338 ◽

Cited By ~ 7

Author(s):

Kentaro Gokita ◽

Jun Inoue ◽

Hiroshi Ishihara ◽

Kazuyuki Kojima ◽

Johji Inazawa

Keyword(s):

Cancer Therapy ◽

Therapeutic Potential

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Adaptation of the group AStreptococcusadhesin Scl1 to bind fibronectin type III repeats within wound‐associated extracellular matrix: implications for cancer therapy

Molecular Microbiology ◽

10.1111/mmi.14317 ◽

2019 ◽

Vol 112 (3) ◽

pp. 800-819 ◽

Cited By ~ 2

Author(s):

Dudley H. McNitt ◽

Soo Jeon Choi ◽

Jessica L. Allen ◽

River A. Hames ◽

Scott A. Weed ◽

...

Keyword(s):

Extracellular Matrix ◽

Cancer Therapy ◽

Type Iii ◽

Fibronectin Type Iii ◽

Fibronectin Type

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Trastuzumab-Targeted Biodegradable Nanoparticles for Enhanced Delivery of Dasatinib in HER2+ Metastasic Breast Cancer

Nanomaterials ◽

10.3390/nano9121793 ◽

2019 ◽

Vol 9 (12) ◽

pp. 1793 ◽

Cited By ~ 4

Author(s):

Enrique Niza ◽

María del Mar Noblejas-López ◽

Iván Bravo ◽

Cristina Nieto-Jiménez ◽

José Antonio Castro-Osma ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Therapy ◽

Therapeutic Potential ◽

Lymphoblastic Leukemia ◽

Philadelphia Chromosome ◽

Breast Cancer Cell Lines ◽

Her2 Positive ◽

Multikinase Inhibitor ◽

Biodegradable Nanoparticles

Dasatinib (DAS) is a multikinase inhibitor that acts on several signaling kinases. DAS is used as a second-line treatment for chronic accelerated myeloid and Philadelphia chromosome-positive acute lymphoblastic leukemia. The therapeutic potential of DAS in other solid tumours is under evaluation. As for many other compounds, an improvement in their pharmacokinetic and delivery properties would potential augment the efficacy. Antibody-targeted biodegradable nanoparticles can be useful in targeted cancer therapy. DAS has shown activity in human epidermal growth factor receptor 2 (HER2) positive tumors, so conjugation of this compound with the anti-HER2 antibody trastuzumab (TAB) with the use of nanocarriers could improve its efficacy. TAB-targeted DAS-loaded nanoparticles were generated by nanotechnology. The guided nanocarriers enhanced in vitro cytotoxicity of DAS against HER2 human breast cancer cell lines. Cellular mechanistic, release studies and nanoparticles stability were undertaken to provide evidences for positioning DAS-loaded TAB-targeted nanoparticles as a potential strategy for further development in HER2-overexpressing breast cancer therapy.

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Roles of MicroRNA-34a in Epithelial to Mesenchymal Transition, Competing Endogenous RNA Sponging and Its Therapeutic Potential

International Journal of Molecular Sciences ◽

10.3390/ijms20040861 ◽

2019 ◽

Vol 20 (4) ◽

pp. 861 ◽

Cited By ~ 9

Author(s):

Dongsong Nie ◽

Jiewen Fu ◽

Hanchun Chen ◽

Jingliang Cheng ◽

Junjiang Fu

Keyword(s):

Cancer Therapy ◽

Cancer Progression ◽

Noncoding Rna ◽

Epithelial To Mesenchymal Transition ◽

Epithelial Mesenchymal Transition ◽

Therapeutic Potential ◽

Circular Rna ◽

Signal Pathways ◽

Competing Endogenous Rna ◽

Mesenchymal Transition

MicroRNA-34a (miR-34a), a tumor suppressor, has been reported to be dysregulated in various human cancers. MiR-34a is involves in certain epithelial-mesenchymal transition (EMT)-associated signal pathways to repress tumorigenesis, cancer progression, and metastasis. Due to the particularity of miR-34 family in tumor-associated EMT, the significance of miR-34a is being increasingly recognized. Competing endogenous RNA (ceRNA) is a novel concept involving mRNA, circular RNA, pseudogene transcript, and long noncoding RNA regulating each other’s expressions using microRNA response elements to compete for the binding of microRNAs. Studies showed that miR-34a is efficient for cancer therapy. Here, we provide an overview of the function of miR-34a in tumor-associated EMT. ceRNA hypothesis plays an important role in miR-34a regulation in EMT, cancer progression, and metastasis. Its potential roles and challenges as a microRNA therapeutic candidate are discussed. As the negative effect on cancer progression, miR-34a should play crucial roles in clinical diagnosis and cancer therapy.

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Targeting Mitochondrial Apoptosis to Overcome Treatment Resistance in Cancer

Cancers ◽

10.3390/cancers12030574 ◽

2020 ◽

Vol 12 (3) ◽

pp. 574 ◽

Cited By ~ 1

Author(s):

Natalie Yan Li Ngoi ◽

Clarice Choong ◽

Joanne Lee ◽

Gregory Bellot ◽

Andrea LA Wong ◽

...

Keyword(s):

Cancer Therapy ◽

Cell Fate ◽

Cancer Progression ◽

Chemotherapy Resistance ◽

Family Members ◽

Biological Significance ◽

Treatment Resistance ◽

B Cell Lymphoma ◽

Lymphocytic Leukemia ◽

Mitochondrial Apoptosis

Deregulated cellular apoptosis is a hallmark of cancer and chemotherapy resistance. The B-cell lymphoma 2 (BCL-2) protein family members are sentinel molecules that regulate the mitochondrial apoptosis machinery and arbitrate cell fate through a delicate balance between pro- and anti-apoptotic factors. The recognition of the anti-apoptotic BCL2 gene as an oncogenic driver in hematological malignancies has directed attention toward unraveling the biological significance of each of the BCL-2 superfamily members in cancer progression and garnered interest in the targeting of apoptosis in cancer therapy. Accordingly, the approval of venetoclax (ABT-199), a small molecule BCL-2 inhibitor, in patients with chronic lymphocytic leukemia and acute myeloid leukemia has become the proverbial torchbearer for novel candidate drug approaches selectively targeting the BCL-2 superfamily. Despite the inspiring advances in this field, much remains to be learned regarding the optimal therapeutic context for BCL-2 targeting. Functional assays, such as through BH3 profiling, may facilitate prediction of treatment response, development of drug resistance and shed light on rational combinations of BCL-2 inhibitors with other branches of cancer therapy. This review summarizes the pathological roles of the BCL-2 family members in cancer, discusses the current landscape of their targeting in clinical practice, and highlights the potential for future therapeutic inroads in this important area.

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