TXNIP Exacerbates the Senescence and Aging-Related Dysfunction of β Cells by Inducing Cell Cycle Arrest Through p38-p16/p21-CDK-Rb Pathway

Li, Yang; Deng, Wenzhen; Wu, Jinlin; He, Qirui; Yang, Gangyi; Luo, Xie; Jia, Yanjun; Yong, Duan; Zhang, Liping; liu, dongfang

doi:10.1089/ars.2021.0224

Cited by 9 publications

(3 citation statements)

References 56 publications

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“…79 Senescent cells often have high expression of at least one of these important cell cycle inhibitors, even though the various senescence-related stimuli engage different signaling pathways. 80 This cell cycle arrest primarily suppresses the replication of cancer cells to restrain the production of a macroscopic tumor or contradictorily contribute to aggressive tumor biology and poor clinical outcome, such as dormancy, stemness, or drug resistance. 81,82 The phosphorylation of H2A.X, commonly known as γH2A.X, is widely detected in cells undergoing diverse modes of senescence.…”

Section: Senescence-associated Nuclear and Chromatin Changesmentioning

confidence: 99%

“…It is noteworthy that p21 can enforce G1 arrest through binding to the cyclin E‐CDK2 and cyclin A‐CDK2 complexes to ensure that Rb is kept hypo‐phosphorylated and active in senescent cells 79 . Senescent cells often have high expression of at least one of these important cell cycle inhibitors, even though the various senescence‐related stimuli engage different signaling pathways 80 . This cell cycle arrest primarily suppresses the replication of cancer cells to restrain the production of a macroscopic tumor or contradictorily contribute to aggressive tumor biology and poor clinical outcome, such as dormancy, stemness, or drug resistance 81,82 …”

Section: Morphological Features Of Senescence and Their Role In Tumor...mentioning

confidence: 99%

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Cellular senescence in cancer: molecular mechanisms and therapeutic targets

Jin,

Duan,

et al. 2024

MedComm

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Aging exhibits several hallmarks in common with cancer, such as cellular senescence, dysbiosis, inflammation, genomic instability, and epigenetic changes. In recent decades, research into the role of cellular senescence on tumor progression has received widespread attention. While how senescence limits the course of cancer is well established, senescence has also been found to promote certain malignant phenotypes. The tumor‐promoting effect of senescence is mainly elicited by a senescence‐associated secretory phenotype, which facilitates the interaction of senescent tumor cells with their surroundings. Targeting senescent cells therefore offers a promising technique for cancer therapy. Drugs that pharmacologically restore the normal function of senescent cells or eliminate them would assist in reestablishing homeostasis of cell signaling. Here, we describe cell senescence, its occurrence, phenotype, and impact on tumor biology. A “one‐two‐punch” therapeutic strategy in which cancer cell senescence is first induced, followed by the use of senotherapeutics for eliminating the senescent cells is introduced. The advances in the application of senotherapeutics for targeting senescent cells to assist cancer treatment are outlined, with an emphasis on drug categories, and the strategies for their screening, design, and efficient targeting. This work will foster a thorough comprehension and encourage additional research within this field.

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Section: Senescence-associated Nuclear and Chromatin Changesmentioning

confidence: 99%

Section: Morphological Features Of Senescence and Their Role In Tumor...mentioning

confidence: 99%

Cellular senescence in cancer: molecular mechanisms and therapeutic targets

Jin,

Duan,

et al. 2024

MedComm

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“…Trx can modulate cellular senescence by modifying the REDOX state of cells and influencing signaling pathways implicated in the initiation and maintenance of senescence [ 61 ]. Deficiency in Trx leads to heightened oxidative stress and DNA damage, which can activate either the p53-p21 or p16-Retinoblastoma protein (Rb) pathways, thereby triggering senescence [ 62 , 63 ]. Moreover, Trx also governs SASP in senescent cells through its regulation of NF-κB, a pivotal transcription factor responsible for controlling the production of inflammatory factors [ 40 , 64 ].…”

Section: The Interplay Between Trx and Cellular Senescencementioning

confidence: 99%

Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases

Yang,

Lin,

Huang

et al. 2024

Redox Biology

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S‐acylation of Ca²⁺ transport proteins in cancer

Kouba,

Demaurex

2024

Chronic Diseases and Translational Medicine

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Alterations in cellular calcium (Ca2+) signals have been causally associated with the development and progression of human cancers. Cellular Ca2+ signals are generated by channels, pumps, and exchangers that move Ca2+ ions across membranes and are decoded by effector proteins in the cytosol or in organelles. S‐acylation, the reversible addition of 16‐carbon fatty acids to proteins, modulates the activity of Ca2+ transporters by altering their affinity for lipids, and enzymes mediating this reversible post‐translational modification have also been linked to several types of cancers. Here, we compile studies reporting an association between Ca2+ transporters or S‐acylation enzymes with specific cancers, as well as studies reporting or predicting the S‐acylation of Ca2+ transporters. We then discuss the potential role of S‐acylation in the oncogenic potential of a subset of Ca2+ transport proteins involved in cancer.

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TXNIP Exacerbates the Senescence and Aging-Related Dysfunction of β Cells by Inducing Cell Cycle Arrest Through p38-p16/p21-CDK-Rb Pathway

Cited by 9 publications

References 56 publications

Cellular senescence in cancer: molecular mechanisms and therapeutic targets

Cellular senescence in cancer: molecular mechanisms and therapeutic targets

Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases

S‐acylation of Ca²⁺ transport proteins in cancer

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TXNIP Exacerbates the Senescence and Aging-Related Dysfunction of β Cells by Inducing Cell Cycle Arrest Through p38-p16/p21-CDK-Rb Pathway

Cited by 9 publications

References 56 publications

Cellular senescence in cancer: molecular mechanisms and therapeutic targets

Cellular senescence in cancer: molecular mechanisms and therapeutic targets

Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases

S‐acylation of Ca2+ transport proteins in cancer

Contact Info

Product

Resources

About

S‐acylation of Ca²⁺ transport proteins in cancer