Overexpression of family with sequence similarity 134, member B (FAM134B) in colon cancers and its tumor suppressive properties in vitro

Lee, Katherine Ting-Wei; Islam, Farhadul; Vider, Jelena; Martin, Jeremy; Chruścik, Anna; Lu, Cu-Tai; Gopalan, Vinod

doi:10.1080/15384047.2020.1810535

Cited by 8 publications

(5 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…FAM134B acts as a tumor suppressor and inhibits cancer growth and proliferation both in vitro and in vivo ( 491 – 494 ). In addition, FAM134B mutations or expression alterations are common in patients with colorectal cancer (CRC), and they are associated with the biological aggressiveness of these cancers ( 491 , 493 , 495 , 496 ).…”

Section: Lysosomal Clearance Of the Er And Related Human Diseasesmentioning

confidence: 99%

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

Reggiori

Molinari

2022

Physiological Reviews

View full text Add to dashboard Cite

ER-phagy (reticulo-phagy) defines the degradation of portions of the endoplasmic reticulum (ER) within lysosomes or vacuoles. It is part of the self-digestion (i.e., auto-phagic) programs recycling cytoplasmic material and organelles, which rapidly mobilize metabolites in cells confronted with nutrient shortage. Moreover, selective clearance of ER subdomains participates to the control of ER size and activity during ER stress, the re-establishment of ER homeostasis after ER stress resolution and the removal of ER parts, in which aberrant and potentially cytotoxic material has been segregated. ER-phagy relies on the individual and/or concerted activation of the ER-phagy receptors, ER peripheral or integral membrane proteins that share the presence of LC3/Atg8-binding motifs in their cytosolic domains. ER-phagy involves the physical separation of portions of the ER from the bulk ER network, and their delivery to the endolysosomal/vacuolar catabolic district. This last step is accomplished by a variety of mechanisms including macro-ER-phagy (in which ER fragments are sequestered by double-membrane autophagosomes that eventually fuse with lysosomes/vacuoles), micro-ER-phagy (in which ER fragments are directly engulfed by endosomes/lysosomes/vacuoles), or direct fusion of ER-derived vesicles with lysosomes/vacuoles. ER-phagy is dysfunctional in specific human diseases and its regulators are subverted by pathogens, highlighting its crucial role for cell and organism life.

show abstract

Section: Lysosomal Clearance Of the Er And Related Human Diseasesmentioning

confidence: 99%

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

Reggiori

Molinari

2022

Physiological Reviews

View full text Add to dashboard Cite

show abstract

“…Three major transducer-based groups have been developed over the last two decades, allowing different bioreceptors to be applied to different biological targets [ 100 ]. Biosensors, such as nano-bioelectronics, are crucial tools to advance the detection of new specific biomarkers that are molecularly relevant to specific types and stages of human diseases [ 106 , 107 ]. Furthermore, nanotechnology plays a crucial role in developing highly sensitive and minimally invasive procedures for detecting trace amounts of biomarkers, particularly in the early stages of neurodegenerative diseases.…”

Section: Discussion Of Biomarker Detectionsmentioning

confidence: 99%

Tau, Glial Fibrillary Acidic Protein, and Neurofilament Light Chain as Brain Protein Biomarkers in Cerebrospinal Fluid and Blood for Diagnosis of Neurobiological Diseases

Park,

KC,

Paneque

et al. 2024

IJMS

View full text Add to dashboard Cite

Neurological damage is the pathological substrate of permanent disability in various neurodegenerative disorders. Early detection of this damage, including its identification and quantification, is critical to preventing the disease’s progression in the brain. Tau, glial fibrillary acidic protein (GFAP), and neurofilament light chain (NfL), as brain protein biomarkers, have the potential to improve diagnostic accuracy, disease monitoring, prognostic assessment, and treatment efficacy. These biomarkers are released into the cerebrospinal fluid (CSF) and blood proportionally to the degree of neuron and astrocyte damage in different neurological disorders, including stroke, traumatic brain injury, multiple sclerosis, neurodegenerative dementia, and Parkinson’s disease. Here, we review how Tau, GFAP, and NfL biomarkers are detected in CSF and blood as crucial diagnostic tools, as well as the levels of these biomarkers used for differentiating a range of neurological diseases and monitoring disease progression. We also discuss a biosensor approach that allows for the real-time detection of multiple biomarkers in various neurodegenerative diseases. This combined detection system of brain protein biomarkers holds significant promise for developing more specific and accurate clinical tools that can identify the type and stage of human neurological diseases with greater precision.

show abstract

“…Studies have uncovered the pivotal role of FAM134B in multiple malignancies. Lee et al [ 20 ] reported that FAM134B may exert anticancer effects by influencing mitochondrial function and inducing cell cycle arrest in colon cancer. FAM134B also acts as a cancer suppressor in breast carcinoma.…”

Section: Discussionmentioning

confidence: 99%

“…Family with sequence similarity 134 member B ( FAM134B ) has been proposed as a cancer suppressor gene[ 18 , 19 ]. Numerous researchers have demonstrated that in colorectal carcinoma, the presence of FAM134B limits the overgrowth and suppresses the proliferation of cancer cells[ 20 , 21 ]. In addition, FAM134B acts as a putative reticulophagy receptor in regulating ER turnover and maintaining calcium homeostasis by remodeling ER[ 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

Suberoylanilide hydroxamic acid upregulates reticulophagy receptor expression and promotes cell death in hepatocellular carcinoma cells

Li,

Tian,

Han

et al. 2023

World J Gastroenterol

View full text Add to dashboard Cite

Esophageal cancer (EC) ranks among the most prevalent malignant tumors affecting the digestive tract. Esophageal squamous cell carcinoma (ESCC) stands as the prevailing pathological subtype, encompassing approximately 90% of all EC patients. In clinical stage II-IVA locally advanced ESCC cases, the primary approach to treatment involves a combination of neoadjuvant therapy and surgical resection. Despite concerted efforts, the long-term outcomes for ESCC patients remain unsatisfactory, with dismal prognoses. However, recent years have witnessed remarkable strides in immunotherapy, particularly in the second- and first-line treatment of advanced or metastatic ESCC, with the development of monoclonal antibodies that inhibit programmed death 1 or programmed death ligand 1 demonstrating encouraging responses and perioperative clinical benefits for various malignancies, including ESCC. This comprehensive review aims to present the current landscape of perioperative immunotherapy for resectable ESCC, focusing specifically on the role of immune checkpoint inhibitors during the perioperative period. Additionally, the review will explore promising biomarkers and offer insights into future prospects.

show abstract

Overexpression of family with sequence similarity 134, member B (FAM134B) in colon cancers and its tumor suppressive properties in vitro

Cited by 8 publications

References 44 publications

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

Tau, Glial Fibrillary Acidic Protein, and Neurofilament Light Chain as Brain Protein Biomarkers in Cerebrospinal Fluid and Blood for Diagnosis of Neurobiological Diseases

Suberoylanilide hydroxamic acid upregulates reticulophagy receptor expression and promotes cell death in hepatocellular carcinoma cells

Contact Info

Product

Resources

About