scholarly journals E26 transformation-specific variant 4 (ETV4) as a tumor promotor in human cancers through specific molecular mechanisms

2021 ◽  
Author(s):  
Wenxiao Jiang ◽  
Yichi Xu ◽  
Xin Chen ◽  
Shuya Pan ◽  
Xueqiong Zhu
Keyword(s):  
Molecular Mechanisms ◽  
Human Cancers ◽  
Tumor Promotor

DLX6-AS1: a putative lncRNA candidate in multiple human cancers

2021 ◽  
Vol 23 ◽  
Author(s):  
Mohsen Sheykhhasan ◽  
Yaghoub Ahmadyousefi ◽  
Reihaneh Seyedebrahimi ◽  
Hamid Tanzadehpanah ◽  
Hamed Manoochehri ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Critical Analysis ◽  
Molecular Mechanisms ◽  
Signalling Pathways ◽  
Biological Functions ◽  
Initial Development ◽  
Human Cancers ◽  
Expression Of Genes ◽  
Non Coding Rnas ◽  
Research Studies

Abstract Long non-coding RNAs (lncRNAs) have important roles in regulating the expression of genes and act as biomarkers in the initial development of different cancers. Increasing research studies have verified that dysregulation of lncRNAs occurs in various pathological processes including tumorigenesis and cancer progression. Among the different lncRNAs, DLX6-AS1 has been reported to act as an oncogene in the development and prognoses of different cancers, by affecting many different signalling pathways. This review summarises and analyses the recent research studies describing the biological functions of DLX6-AS1, its overall effect on signalling pathways and the molecular mechanisms underlying its action on the expression of genes in multiple human cancers. Our critical analysis suggests that different signalling pathways associated to this lncRNA may be used as a biomarker for diagnosis, or targets of treatment in cancers.

scholarly journals TRIM proteins in neuroblastoma

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Yonghu Xu ◽  
Zihan Zhang ◽  
Guofeng Xu
Keyword(s):  
High Risk ◽  
Tumor Suppressor ◽  
Solid Tumor ◽  
Molecular Mechanisms ◽  
Tumor Suppressor Proteins ◽  
Human Cancers ◽  
Tripartite Motif ◽  
Tumor In Childhood ◽  
Trim Proteins

Abstract Neuroblastoma (NB) is the most common extracranial solid tumor in childhood. Outcome for children with high-risk NB remains unsatisfactory. Accumulating evidence suggests that tripartite motif (TRIM) family proteins express diversely in various human cancers and act as regulators of oncoproteins or tumor suppressor proteins. This review summarizes the TRIM proteins involving in NB and the underlying molecular mechanisms. We expect these new insights will provide important implications for the treatment of NB by targeting TRIM proteins.

scholarly journals Exploring the Biological Activity and Mechanism of Xenoestrogens and Phytoestrogens in Cancers: Emerging Methods and Concepts

2021 ◽  
Vol 22 (16) ◽  
pp. 8798
Author(s):  
Xiaoqiang Wang ◽  
Desiree Ha ◽  
Ryohei Yoshitake ◽  
Yin S. Chan ◽  
David Sadava ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Extensive Literature ◽  
Industrial Chemicals ◽  
Therapeutic Approaches ◽  
Human Cancers ◽  
Systemic Level ◽  
Critical Timing ◽  
New Applications ◽  
Female Lifespan

Xenoestrogens and phytoestrogens are referred to as “foreign estrogens” that are produced outside of the human body and have been shown to exert estrogen-like activity. Xenoestrogens are synthetic industrial chemicals, whereas phytoestrogens are chemicals present in the plant. Considering that these environmental estrogen mimics potentially promote hormone-related cancers, an understanding of how they interact with estrogenic pathways in human cells is crucial to resolve their possible impacts in cancer. Here, we conducted an extensive literature evaluation on the origins of these chemicals, emerging research techniques, updated molecular mechanisms, and ongoing clinical studies of estrogen mimics in human cancers. In this review, we describe new applications of patient-derived xenograft (PDX) models and single-cell RNA sequencing (scRNA-seq) techniques in shaping the current knowledge. At the molecular and cellular levels, we provide comprehensive and up-to-date insights into the mechanism of xenoestrogens and phytoestrogens in modulating the hallmarks of cancer. At the systemic level, we bring the emerging concept of window of susceptibility (WOS) into focus. WOS is the critical timing during the female lifespan that includes the prenatal, pubertal, pregnancy, and menopausal transition periods, during which the mammary glands are more sensitive to environmental exposures. Lastly, we reviewed 18 clinical trials on the application of phytoestrogens in the prevention or treatment of different cancers, conducted from 2002 to the present, and provide evidence-based perspectives on the clinical applications of phytoestrogens in cancers. Further research with carefully thought-through concepts and advanced methods on environmental estrogens will help to improve understanding for the identification of environmental influences, as well as provide novel mechanisms to guide the development of prevention and therapeutic approaches for human cancers.

scholarly journals Recombinant immunotoxins development for HER2-based targeted cancer therapies

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Reza Mahmoudi ◽  
Hassan Dianat-Moghadam ◽  
Mansour Poorebrahim ◽  
Samaneh Siapoush ◽  
Vahdat Poortahmasebi ◽  
...  
Keyword(s):  
Cancer Biology ◽  
Molecular Mechanisms ◽  
Tyrosine Kinase Receptor ◽  
Tumor Biomarker ◽  
Cancer Therapies ◽  
Complementary Method ◽  
Human Cancers ◽  
Drug Conjugates ◽  
Recombinant Immunotoxins ◽  
Her2 Signaling

AbstractUnderstanding the molecular mechanisms of cancer biology introduces targeted therapy as a complementary method along with other conventional therapies. Recombinant immunotoxins are tumor specific antibodies that their recognizing fragment is utilized for delivering modified toxins into tumor cells. These molecules have been considered as a targeted strategy in the treatment of human cancers. HER2 tumor biomarker is a transmembrane tyrosine kinase receptor that can be used for targeted therapies in the forms of anti-HER2 monoclonal antibodies, antibody–drug conjugates and immunotoxins. There have been many studies on HER2-based immunotoxins in recent years, however, little progress has been made in the clinical field which demanded more improvements. Here, we summarized the HER2 signaling and it’s targeting using immunotherapeutic agents in human cancers. Then, we specifically reviewed anti-HER2 immunotoxins, and their strengths and drawbacks to highlight their promising clinical impact.

scholarly journals Rho GTPase–independent regulation of mitotic progression by the RhoGEF Net1

2013 ◽  
Vol 24 (17) ◽  
pp. 2655-2667 ◽  
Author(s):  
Sarita Menon ◽  
Wonkyung Oh ◽  
Heather S. Carr ◽  
Jeffrey A. Frost
Keyword(s):  
Molecular Mechanisms ◽  
Spindle Assembly Checkpoint ◽  
Rho Gtpase ◽  
Spindle Assembly ◽  
Nucleotide Exchange ◽  
Altered Expression ◽  
Human Cancers ◽  
Nucleotide Exchange Factor ◽  
Chromosome Congression ◽  
P21 Activated Kinase

Neuroepithelial transforming gene 1 (Net1) is a RhoA-subfamily–specific guanine nucleotide exchange factor that is overexpressed in multiple human cancers and is required for proliferation. Molecular mechanisms underlying its role in cell proliferation are unknown. Here we show that overexpression or knockdown of Net1 causes mitotic defects. Net1 is required for chromosome congression during metaphase and generation of stable kinetochore microtubule attachments. Accordingly, inhibition of Net1 expression results in spindle assembly checkpoint activation. The ability of Net1 to control mitosis is independent of RhoA or RhoB activation, as knockdown of either GTPase does not phenocopy effects of Net1 knockdown on nuclear morphology, and effects of Net1 knockdown are effectively rescued by expression of catalytically inactive Net1. We also observe that Net1 expression is required for centrosomal activation of p21-activated kinase and its downstream kinase Aurora A, which are critical regulators of centrosome maturation and spindle assembly. These results identify Net1 as a novel regulator of mitosis and indicate that altered expression of Net1, as occurs in human cancers, may adversely affect genomic stability.

scholarly journals GPRC5A: An Emerging Biomarker in Human Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Xiaoxia Jiang ◽  
Xin Xu ◽  
Mengjie Wu ◽  
Zhonghai Guan ◽  
Xingyun Su ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
G Protein ◽  
Molecular Mechanisms ◽  
Lung Tumor ◽  
Human Cancer ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Aberrant Expression ◽  
Human Cancers ◽  
G Protein Coupled

Aberrant expression of G protein-coupled receptors (GPCRs) is frequently associated with tumorigenesis. G Protein-coupled receptor class C group 5 member A (GPRC5A) is a member of the GPCR superfamily, is expressed preferentially in lung tissues, and is regulated by various entities at multiple levels. GPRC5A exerts a tumor suppressive role in lung cancer and GPRC5A deletion promotes lung tumor initiation and progression. Recent advances have highlighted that GPRC5A dysregulation is found in various human cancers and is related to many tumor-associated signaling pathways, including the cyclic adenosine monophosphate (cAMP), nuclear factor (NF)-κB, signal transducer and activator of transcription (STAT) 3, and focal adhesion kinase (FAK)/Src signaling. This review aimed to summarize our updated view on the biology and regulation of GPRC5A, its expression in human cancers, and the linked signaling pathways. A better comprehension of the underlying cellular and molecular mechanisms of GPRC5A will provide novel insights into its potential diagnostic and therapeutic value.

Molecular mechanisms involved in DNA repair in human cancers: An overview of PI3k/Akt signaling and PIKKs crosstalk

2021 ◽  
Author(s):  
Forough Alemi ◽  
Aydin Raei sadigh ◽  
Faezeh Malakoti ◽  
Yusuf Elhaei ◽  
Seyed Hamed Ghaffari ◽  
...  
Keyword(s):  
Dna Repair ◽  
Molecular Mechanisms ◽  
Akt Signaling ◽  
Human Cancers

scholarly journals KCNQ1OT1: An Oncogenic Long Noncoding RNA

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1602
Author(s):  
Patrice Cagle ◽  
Qi Qi ◽  
Suryakant Niture ◽  
Deepak Kumar
Keyword(s):  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Vital Role ◽  
Migration And Invasion ◽  
Biological Functions ◽  
Aberrant Expression ◽  
Human Cancers ◽  
Oral Melanoma ◽  
Opposite Strand

Long noncoding RNAs (lncRNAs) are transcripts greater than 200 nucleotides that do not code for proteins but regulate gene expression. Recent studies indicate that lncRNAs are involved in the modulation of biological functions in human disease. KCNQ1 Opposite Strand/Antisense Transcript 1 (KCNQ1OT1) encodes a lncRNA from the opposite strand of KCNQ1 in the CDKN1C/KCNQ1OT1 cluster that is reported to play a vital role in the development and progression of cancer. KCNQ1OT1 regulates cancer cell proliferation, cell cycle, migration and invasion, metastasis, glucose metabolism, and immune evasion. The aberrant expression of KCNQ1OT1 in cancer patients is associated with poor prognosis and decreased survival. This review summarizes recent literature related to the biological functions and molecular mechanisms of KCNQ1OT1 in various human cancers, including colorectal, bladder, breast, oral, melanoma, osteosarcoma, lung, glioma, ovarian, liver, acute myeloid leukemia, prostate, and gastric. We also discuss the role of KCNQ1OT1 as a promising diagnostic biomarker and a novel therapeutic target in human cancers.

scholarly journals Esophageal Cancer: Insights from Mouse Models

2015 ◽  
Vol 8s1 ◽  
pp. CGM.S21218 ◽  
Author(s):  
Marie-Pier Tétreault
Keyword(s):  
Esophageal Cancer ◽  
Mouse Models ◽  
Molecular Mechanisms ◽  
Human Subjects ◽  
Surgical Techniques ◽  
Therapeutic Strategies ◽  
Human Cancers ◽  
Genetic Modifications ◽  
Wide Range ◽  
Gestation Time

Esophageal cancer is the eighth leading cause of cancer and the sixth most common cause of cancer-related death worldwide. Despite recent advances in the development of surgical techniques in combination with the use of radiotherapy and chemotherapy, the prognosis for esophageal cancer remains poor. The cellular and molecular mechanisms that drive the pathogenesis of esophageal cancer are still poorly understood. Hence, understanding these mechanisms is crucial to improving outcomes for patients with esophageal cancer. Mouse models constitute valuable tools for modeling human cancers and for the preclinical testing of therapeutic strategies in a manner not possible in human subjects. Mice are excellent models for studying human cancers because they are similar to humans at the physiological and molecular levels and because they have a shorter gestation time and life cycle. Moreover, a wide range of well-developed technologies for introducing genetic modifications into mice are currently available. In this review, we describe how different mouse models are used to study esophageal cancer.

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