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The TMEM family is widely distributed in the plasma membrane and organelle membrane, and has multiple biological functions. The TMEM family has different functions and mechanisms of action in different diseases. Recent research shows that TMEM family members play an important role in the pathogenesis of non tumor diseases, especially in cardiovascular, respiratory and nervous system diseases, such as atherosclerosis, Parkinson′s disease, depression, etc. This article reviews the mechanism of action of the TMEM family in non tumor diseases, which is of great significance for further revealing the disease mechanism and elucidating the biological functions of TMEM family members, and provides a new perspective for disease treatment strategies.

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BACKGROUND: The aim was to evaluate the causes of death for patients with localized, regional and metastatic penile cancer (PeCa) after diagnosis. METHODS: PeCa patients diagnosed during 2004-2018 in the Surveillance, Epidemiology, and End Results program database were identified. Causes of deaths including PeCa, second malignant tumors (SMTs) and non-tumor diseases were analyzed, as well as the standardized mortality ratio (SMR) of each cause. RESULTS: For localized PeCa, 800 of 2155 patients died during the follow-up. 24.9% of all deaths were due to PeCa. 18.0% and 57.1% deaths were due to SMTs and non-tumor causes. Main SMTs included cancers of lung and bronchus (n = 40) and skin (n = 11) with significantly increased SMRs of 1.71 (1.22-2.33) and 4.82 (2.41-8.63). Mortality risks of other SMTs were mostly similar with the general populations. Main causes of non-tumor diseases included diseases of heart [n = 172, SMR: 1.66 (1.42-1.93)], COPD and allied cond [n = 38, SMR: 1.63 (1.15-2.24)], and cerebrovascular diseases [n = 33, SMR: 1.71 (1.17-2.4)]. For regional PeCa, 679 of 1310 patients died including 43.5% PeCa, 14.8% SMTs and 26.6% non-tumor causes. The mortality risks of cancers from lung and bronchus [SMR: 2.41 (1.53-3.62)], skin [SMR: 6.41 (2.35-13.95)] and testis [SMR: 149.35 (18.09-539.5)] were significantly increased. Main non-tumor causes of death included diseases of heart [n = 71, SMR: 1.77 (1.38-2.23)], COPD and allied cond [n = 17, SMR: 1.85 (1.08-2.95)] and diabetes mellitus [n = 16, SMR: 3.62 (2.07-5.88)]. For distant diseases, 109 of 132 patients died including 76 (69.7%) died for PeCa itself, 24 (22.0%) died for SMTs and 9 (8.3%) died for non-tumor diseases. The majority of PeCa deaths (67.1%) and SMTs deaths (79.2%) occurred within 1 year after the diagnosis of PeCa. CONCLUSIONS: We firstly analyzed the SMTs and non-tumor causes of death and morality risks of each cause for PeCa patients, which provided valuable information for PeCa patients on disease prevention and health care during their survivorship.

Asunto(s)

Neoplasias del Pene , Enfermedad Pulmonar Obstructiva Crónica , Masculino , Humanos , Causas de Muerte , Supervivencia , Factores de Riesgo

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CircRNA E3 ubiquitin protein ligase (ITCH) (circRNA ITCH, circ-ITCH), a stable closed-loop RNA derived from the 20q11.22 region of chromosome 20, is a new circRNA discovered in the cytoplasm in recent decades. Studies have shown that it does not encode proteins, but regulates proteins expression at different levels. It is down-regulated in tumor diseases and is involved in a number of biological activities, including inhibiting cell proliferation, migration, invasion, and promoting apoptosis. It can also alter disease progression in non-tumor disease by affecting the cell cycle, inflammatory response, and critical proteins. Circ-ITCH also holds a lot of promise in terms of tumor and non-tumor clinical diagnosis, prognosis, and targeted therapy. As a result, in order to aid clinical research in the hunt for a new strategy for diagnosing and treating human diseases, this study describes the mechanism of circ-ITCH as well as its clinical implications.

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The N6-methyladenosine (m6A) modification is the most abundant internal modification of messenger RNA (mRNA) in higher eukaryotes. Under the actions of methyltransferase, demethylase and methyl-binding protein, m6A resulting from RNA methylation becomes dynamic and reversible, similar to that from DNA methylation, and this effect allows the generated mRNA to participate in metabolism processes, such as splicing, transport, translation, and degradation. The most common tumors are those found in the gastrointestinal tract, and research on these tumors has flourished since the discovery of m6A. Overall, further analysis of the mechanism of m6A and its role in tumors may contribute to new ideas for the treatment of tumors. m6A also plays an important role in non-tumor diseases of the gastrointestinal tract. This manuscript reviews the current knowledge of m6A-related proteins, mRNA metabolism and their application in gastrointestinal tract disease.

RESUMEN

S100A10 is a small molecular weight protein expressed in the cytoplasm of many cells and one of the members of the S100 protein family that binds calcium and forms the largest subgroup of EF-hand proteins. The regulatory processes of S100A10 are complicated. S100A10 participates in the regulation of a variety of tumor and non-tumor diseases through cascade reactions with multitudinous signaling molecules. In malignant tumors, such as acute promyelocytic leukemia (APL) and lung cancer, S100A10 is likely involved in their progression, including invasion and metastasis through the regulation of plasmin production and subsequent plasmin-dependent stimulation of other proteases, such as matrix metalloproteinase (MMP)-2 and -9. Both the plasmin and MMPs are capable of inducing degradation of the extracellular matrix (ECM) and basement membrane, which is a critical step for tumor progression. In non-tumor diseases, the distribution of S100A10 in the brain and its interaction with 5-hydroxytryptamine 1B (5-HT1B) receptor, an important mediator in the central nervous system that maintains a dynamic balance of the neurotransmitters, correlates with depression-like behavior. S100A10 also participates in inflammatory responses through the regulation of peripheral macrophage migration to the inflammatory sites, which depends on the generation of plasmin and other proteinases at the surface of macrophages. Considerable attention should be paid to understand the significant role of S100A10 in the modulation of malignant tumor and non-tumor diseases.