Volume 4 (2020)

PRMT5 function and targeting in cancer

Hyungsoo Kim1 and Ze’ev A. Ronai1

Protein methyl transferases play critical roles in numerous regulatory pathways that underlie cancer development, progression and therapy-response. Here we discuss the function of PRMT5, a member of the nine-member PRMT family, in controlling oncogenic processes including tumor intrinsic, as well as extrinsic microenvironmental signaling pathways. We discuss PRMT5 effect on histone methylation and methylation of regulatory proteins including those involved in RNA splicing, cell cycle, cell death and metabolic signaling. In all, we highlight the importance of PRMT5 regulation and function in cancer, which provide the foundation for therapeutic modalities targeting PRMT5.

Regulation of immune checkpoint blockade efficacy in breast cancer by FIP200: A canonical-autophagy-independent function

Syn Kok Yeo1 and Jun-Lin Guan1

DISSECTING THE ROLE OF AUTOPHAGY AND AUTOPHAGY-INDEPENDENT FUNCTIONS OF FIP200 IN BREAST CANCER Although initial studies of autophagy genes in cancer implicated a tumor suppressive role, it has become apparent

Exploiting the circuit breaker cancer evolution model in human clear cell renal cell carcinoma

James J. Hsieh1 and Emily H. Cheng2,3,4

INTRODUCTION On average a human adult body encompasses fifty trillion cells (~5×1013) with a daily turnover of hundred billion cells (~1011) within which each contains two copies of ~three billion

High mitochondrial calcium levels precede neuronal death in vivo in Alzheimer’s disease

Maria Calvo-Rodriguez1 and Brian J. Bacskai1

MITOCHONDRIAL CALCIUM OVERLOAD AFTER PLAQUE DEPOSITION Ca2+ is essential for the normal function of mitochondrial activity, and therefore Ca2+ levels are tightly regulated in mitochondria. However, excessive levels of Ca2+

The role of lipids in autophagy and its implication in neurodegeneration

Sergio Hernandez-Diaz1,2 and Sandra-Fausia Soukup1,2

Neurodegenerative diseases are, at present, major socio-economic burdens without effective treatments and their increasing prevalence means that these diseases will be a challenge for future generations. Neurodegenerative diseases may differ in etiology and pathology but are often caused by the accumulation of dysfunctional and aggregation-prone proteins. Autophagy, a conserved cellular mechanism, deals with cellular stress and waste product build-up and has been shown to reduce the accumulation of dysfunctional proteins in animal models of neurodegenerative diseases. Historically, progress in understanding the precise function of lipids has traditionally been far behind other biological molecules (like proteins) but emerging works demonstrate the importance of lipids in the autophagy pathway and how the disturbance of lipid metabolism is connected to neurodegeneration. Here we review how altered autophagy and the disturbance of lipid metabolism, particularly of phosphoinositols and sphingolipids, feature in neurodegenerative diseases and address work from the field that suggests that these potentially offer an opportunity of therapeutic intervention.

Immune system activation by natural products and complex fractions: a network pharmacology approach in cancer treatment

Alejandra Gomez-Cadena1,2,3, Alfonso Barreto3, Susana Fiorentino3 and Camilla Jandus1,2

INTRODUCTION Over the past decade, immunotherapy has become a promising approach to treat cancer and is now being combined with standard chemotherapy and immune response activators to improve the outcome

Mitochondria, mitophagy, and metabolic disease: towards assembling the puzzle

Zhiyong Chen1, Marine Berquez1 and Alessandro Luciani1

Mitochondria — the intracellular powerhouse that stores energy and signaling metabolites — are highly dynamic, double-membrane organelles that enact metabolism, hence sustaining physiology and organismal health. The maintenance of these

Mitochondria in cancer

Debora Grasso1, Luca X. Zampieri1, Tânia Capelôa1, Justine A. Van de Velde1 and Pierre Sonveaux1

The rediscovery and reinterpretation of the Warburg effect in the year 2000 occulted for almost a decade the key functions exerted by mitochondria in cancer cells. Until recent times, the scientific community indeed focused on constitutive glycolysis as a hallmark of cancer cells, which it is not, largely ignoring the contribution of mitochondria to the malignancy of oxidative and glycolytic cancer cells, being Warburgian or merely adapted to hypoxia. In this review, we highlight that mitochondria are not only powerhouses in some cancer cells, but also dynamic regulators of life, death, proliferation, motion and stemness in other types of cancer cells. Similar to the cells that host them, mitochondria are capable to adapt to tumoral conditions, and probably to evolve to ‘oncogenic mitochondria’ capable of transferring malignant capacities to recipient cells. In the wider quest of metabolic modulators of cancer, treatments have already been identified targeting mitochondria in cancer cells, but the field is still in infancy.

HIF1α or mitophagy: which drives cardiomyocyte differentiation?

Beatriz Villarejo-Zori1,#, Juan Ignacio Jiménez-Loygorri1,# and Patricia Boya1

Cardiomyocytes (CMs) are the main cellular component of the heart's atria and ventricles, and their contractile capacity is the engine that drives blood flow throughout the body. The differentiation of

Exocytotic fusion pore under stress

Helena Haque Chowdhury1,2 and Robert Zorec1,2

Exocytosis is a universal process of eukaryotic cells, consisting of fusion between the vesicle and the plasma membranes, leading to the formation of a fusion pore, a channel through which vesicle cargo exits into the extracellular space. In 1986, Rand and Parsegian proposed several stages to explain the nature of membrane fusion. Following stimulation, it starts with focused stress destabilization of membranes in contact, followed by the coalescence of two membrane surfaces. In the next fraction of a millisecond, restabilization of fused membranes is considered to occur to maintain the cell's integrity. This view predicted that once a fusion pore is formed, it must widen abruptly, irreversibly and fully, whereby the vesicle membrane completely integrates with and collapses into the plasma membrane (full fusion exocytosis). However, recent experimental evidence has revealed that once the fusion pore opens, it may also reversibly close (transient or kiss-and-run exocytosis). Here, we present a historical perspective on understanding the mechanisms that initiate (...)

Targeting immune-checkpoint inhibitor resistance mechanisms by MEK inhibitor and agonist anti-CD40 antibody combination therapy

Daniel Baumann1,2 and Rienk Offringa1,2

– [table id=351/] IDENTIFYING SUITABLE CYTOSTATIC DRUGS FOR COMBINATORIAL IMMUNOTHERAPY The main dilemma in finding combinations of cytostatic and immunostimulatory drugs that act synergistically is as follows. On the one

Hyaluronan goes to great length

Vera Gorbunova1, Masaki Takasugi1 and Andrei Seluanov1

The naked mole rat is the longest-lived rodent with the maximum lifespan of over 35 years. Naked mole rats are protected from a wide range of age-related diseases including cancer,

PRMT5 function and targeting in cancer

Hyungsoo Kim1 and Ze’ev A. Ronai1

Protein methyl transferases play critical roles in numerous regulatory pathways that underlie cancer development, progression and therapy-response. Here we discuss the function of PRMT5, a member of the nine-member PRMT family, in controlling oncogenic processes including tumor intrinsic, as well as extrinsic microenvironmental signaling pathways. We discuss PRMT5 effect on histone methylation and methylation of regulatory proteins including those involved in RNA splicing, cell cycle, cell death and metabolic signaling. In all, we highlight the importance of PRMT5 regulation and function in cancer, which provide the foundation for therapeutic modalities targeting PRMT5.

Regulation of immune checkpoint blockade efficacy in breast cancer by FIP200: A canonical-autophagy-independent function

Syn Kok Yeo1 and Jun-Lin Guan1

DISSECTING THE ROLE OF AUTOPHAGY AND AUTOPHAGY-INDEPENDENT FUNCTIONS OF FIP200 IN BREAST CANCER Although initial studies of autophagy genes in cancer implicated a tumor suppressive role, it has become apparent

Exploiting the circuit breaker cancer evolution model in human clear cell renal cell carcinoma

James J. Hsieh1 and Emily H. Cheng2,3,4

INTRODUCTION On average a human adult body encompasses fifty trillion cells (~5×1013) with a daily turnover of hundred billion cells (~1011) within which each contains two copies of ~three billion

Fine intercellular connections in development: TNTs, cytonemes, or intercellular bridges?

Olga Korenkova1,2, Anna Pepe1 and Chiara Zurzolo1

Intercellular communication is a fundamental property of multicellular organisms, necessary for their adequate responses to changing environment. Tunneling nanotubes (TNTs) represent a novel means of intercellular communication being a long cell-to-cell conduit. TNTs are actively formed under a broad range of stresses and are also proposed to exist under physiological conditions. Development is a physiological condition of particular interest, as it requires fine coordination. Here we discuss whether protrusions shown to exist during embryonic development of different species could be TNTs or if they represent other types of cell structure, like cytonemes or intercellular bridges, that are suggested to play an important role in development.

Kynurenine: an oncometabolite in colon cancer

Niranjan Venkateswaran1 and Maralice Conacci-Sorrell1,2,3

TRYPTOPHAN IS PREFERENTIALLY CONVERTED INTO KYNURENINE IN COLON CANCER Tryptophan can be utilized in three ways intracellularly: it can be incorporated into newly synthesized proteins, it can be processed by

Fatty acids – from energy substrates to key regulators of cell survival, proliferation and effector function

Danilo Cucchi1, Dolores Camacho-Muñoz2, Michelangelo Certo3, Valentina Pucino3, Anna Nicolaou2,4 and Claudio Mauro3,5,6

Recent advances in immunology and cancer research show that fatty acids, their metabolism and their sensing have a crucial role in the biology of many different cell types. Indeed, they are able to affect cellular behaviour with great implications for pathophysiology. Both the catabolic and anabolic pathways of fatty acids present us with a number of enzymes, receptors and agonists/antagonists that are potential therapeutic targets, some of which have already been successfully pursued. Fatty acids can affect the differentiation of immune cells, particularly T cells, as well as their activation and function, with important consequences for the balance between anti- and pro-inflammatory signals in immune diseases, such as rheumatoid arthritis, psoriasis, diabetes, obesity and cardiovascular conditions. In the context of cancer biology, fatty acids mainly provide substrates for (…)

A sympathetic gut connection drives the metabolic benefits of Roux-en-Y gastric bypass

Mohammed K. Hankir1

Surgery is regarded by many as the go-to treatment option for severe obesity; yet how physically altering the gastrointestinal tract produces such striking results on body weight and overall metabolic health is poorly understood. In a recent issue of Cell Reports Ye et al. (2020) compare mouse models of Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG), the two most commonly performed weight loss surgeries in the clinic today, to show that the former reconfiguring procedure selectively increases resting metabolic rate through splanchnic nerve-mediated browning of mesenteric white fat. More significantly, they demonstrate that this effect for RYGB is required for the maintained negative energy balance and improved glycemic control that it confers.

Exploiting the circuit breaker cancer evolution model in human clear cell renal cell carcinoma

James J. Hsieh1 and Emily H. Cheng2,3,4

INTRODUCTION On average a human adult body encompasses fifty trillion cells (~5×1013) with a daily turnover of hundred billion cells (~1011) within which each contains two copies of ~three billion

HIF1α or mitophagy: which drives cardiomyocyte differentiation?

Beatriz Villarejo-Zori1,#, Juan Ignacio Jiménez-Loygorri1,# and Patricia Boya1

Cardiomyocytes (CMs) are the main cellular component of the heart's atria and ventricles, and their contractile capacity is the engine that drives blood flow throughout the body. The differentiation of

Copper – a novel stimulator of autophagy

Hans Zischka1,2 and Guido Kroemer3-7

In biomedicine, the transition metal copper has a Janus-faced dual role, as an essential but static cofactor of vital enzymes but also as a highly detrimental poison, if in excess.

Coronavirus infections: Epidemiological, clinical and immunological features and hypotheses

Didier Raoult1, Alimuddin Zumla2,3, Franco Locatelli4, Giuseppe Ippolito5 and Guido Kroemer6-10,*

INTRODUCTION Infections have been limiting quality of life and longevity throughout human history. Endemic infections have been associated to a significant number of avoidable deaths and a significant increase of

ACBP is an appetite stimulator across phylogenetic barriers

Frank Madeo1,2, Nektarios Tavernarakis3,4, José M. Bravo-San Pedro5-7,# and Guido Kroemer5-10,#

Human civilization is unique with respect to the organization of our natural environment, allowing constant supply of nutrients to most individuals in developed countries, contrasting with the natural fluctuation in

Necroptosis, tumor necrosis and tumorigenesis

Zheng-gang Liu1 and Delong Jiao1

INTRODUCTION Cell death can happen through either an active, regulated process, known as programmed cell death, or a passive, uncontrolled course. Because of the dramatic morphological differences of these two