Involvement of F-BOX proteins in progression and development of human malignancies

Uddin, Shahab; Bhat, Ajaz A.; Krishnankutty, Roopesh; Mir, Fayaz Ahmad; Kuliński, Michał; Mohammad, Ramzi M.

doi:10.1016/j.semcancer.2015.09.008

Cited by 48 publications

(37 citation statements)

References 230 publications

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“…Tumor progression is the last phase during tumor development and is characterized by increased growth speed and invasiveness, as well as phenotypic alterations . β‐arrestin 2 enhances cell viability by downregulating FOXO1, whereas siRNA‐mediated β‐arrestin 2 silencing lowers cell viability and tumor metastasis, which is correlated with increased FOXO1 activity .…”

Section: Anticancer Mechanisms Of Foxo1mentioning

confidence: 99%

Deciphering the roles of FOXO1 in human neoplasms

Jiang

Tian

Yang

et al. 2018

Intl Journal of Cancer

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Neoplasms constituted an enormous burden and contributed to an estimated 8.2 million deaths in 2012 worldwide. FOXO1 (forkhead box O1), a member of the forkhead box (FOX) family, is a transcriptional factor involved in diverse cellular functions. Herein, we concentrate on recent studies of the antineoplastic roles of FOXO1 in neoplasms. This article may serve as a guide for future research and identify FOXO1 as a potent therapeutic target in neoplasms.

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Section: Anticancer Mechanisms Of Foxo1mentioning

confidence: 99%

Deciphering the roles of FOXO1 in human neoplasms

Jiang

Tian

Yang

et al. 2018

Intl Journal of Cancer

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“…Previous reports described an association between abnormal levels of the myeloid cell leukemia 1 (MCL1) protein and the development of some cancers (27,28,31). However, scientific studies do not suggest a link between the level of MCL1 protein expression in HTLV-1-infected cells and the pathogenesis of adult T-cell leukemia (ATL) has not been studied.…”

Section: Resultsmentioning

confidence: 99%

“…There is a lot of evidence to suggest that abnormal expression of the MCL1 protein contributes to the progression of human cancers, including prostate, breast, ovarian, and cervical cancers as well as melanoma and leukemia (27,28,31). Moreover, knockdown of MCL1 expression using an shRNA system in several cancer cell lines resulted in a remarkable inhibition of tumor growth (47).…”

Section: Figmentioning

confidence: 99%

Enhanced Stabilization of MCL1 by the Human T-Cell Leukemia Virus Type 1 bZIP Factor Is Modulated by Blocking the Recruitment of Cullin 1 to the SCF Complex

Mukai

Ohshima

2016

Molecular and Cellular Biology

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Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that is the etiological agent of adult T-cell leukemia (ATL). The HTLV-1 basic leucine zipper factor (HBZ), which is encoded by the minus strand of the provirus, is constitutively expressed in all ATL patient cells and likely contributes to the development and maintenance of ATL. Furthermore, the overexpression of the myeloid cell leukemia 1 (MCL1) protein is frequently observed in hematological cancers as well as several other types of cancers. Here, we found that the expression of HBZ in cells stabilized MCL1 protein expression and suppressed the MCL1-mediated release of cytochrome c from the mitochondria. This effect was mediated by inhibition of the ubiquitin-dependent degradation of MCL1. In a serial binding assay, HBZ interacted with cullin 1 (CUL1) through a head-to-tail interaction. The association between CUL1 and Skp1, which serves as the molecular scaffold for the components of SCF ubiquitin ligase complexes, was markedly repressed in the presence of HBZ. Mechanistic analysis indicated that HBZ abrogated the CUL1 association with Skp1, which in turn promoted the cellular expression of MCL1. This novel function of HBZ likely plays a role in the viral pathogenesis of HTLV-1 and provides important insights into our understanding of the development of ATL.H uman T-cell leukemia virus type 1 (HTLV-1) infects at least 5 million to 10 million people worldwide and is the causative agent of adult T-cell leukemia (ATL) (1-4). In most cases, HTLV-1 infection is transmitted through breast milk, blood cells, and dendritic cells in vivo (5). The majority of HTLV-1 carriers do not develop any significant clinical symptoms throughout their lives; however, approximately 5% of HTLV-1-infected subjects progress to ATL (6). Although ATL was discovered 40 years ago, there is still no effective treatment for this disease, in part because the underlying mechanisms of HTLV-1-mediated oncogenesis have not been fully elucidated.The HTLV-1 genome encodes three common retroviral structural and enzymatic proteins (gag, pol, and env proteins) and is flanked by long terminal repeats (LTR) at each end. There is a pX region located between the env gene and the 3= LTR (7). The plus strand of the pX region encodes regulatory and accessory proteins, including p12 I , p21 I , p13 II , p30 II , Rex, and Tax (7). It is well established that the Tax protein is a potent oncoprotein that either strongly activates or inactivates the transcription of target genes as well as interacts with numerous cellular factors that promote the survival and immortalization of HTLV-1-infected T cells (8-13). Interestingly, the Tax protein was detected in only 40% of ATL cases (14, 15) due to nonsense mutations, insertions, deletions, and epigenetic alterations, such as DNA methylation and histone modifications of the 5= LTR of the HTLV-1 provirus (16)(17)(18)(19). These studies suggested that Tax is required for the virus to enhance viral spreading during the earliest stage of HTLV-1 infec...

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“…Jang and co‐workers identified the S‐phase kinase‐associated protein‐2 (SKP2) as a novel YAP target. SKP2 (also called F‐box and leucine‐rich repeat protein‐1; FBXL1) is an F‐box protein of the Skp1‐Cullin1‐F‐box (SCF) ubiquitin ligase complex that targets the cell cycle inhibitors p27 and p21 for proteasomal degradation and thereby promotes cell cycle entry and G1/S transition (Uddin et al , ). Contrary to previous studies that attributed the high SKP2 protein levels in different human cancers to an increased protein stability, Jang and co‐workers found that Skp2 mRNA levels are regulated by mechanical cues such as cell attachment and ECM rigidity and depend on the translocation and activation of YAP, as YAP depletion results in reduced SKP2 and increased p21 and p27 levels (Fig ; Jang et al , ).…”

Section: Yap‐dependent Transcriptional Regulation Drives Cancer Formamentioning

confidence: 99%

A forceful connection: mechanoregulation of oncogenic YAP

2017

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The Yes‐associated protein (YAP) is an important transcriptional co‐activator that mediates the cellular response to mechanical and cytoskeletal cues. In two recent papers published in The EMBO Journal, Dae‐Sik Lim and colleagues show how YAP activity affects cancer formation and metastasis via a crosstalk with myocardin‐related transcription factors (MRTFs; Kim et al, 2017) and SKP2‐dependent cell cycle progression (Jang et al, 2017).

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Involvement of F-BOX proteins in progression and development of human malignancies

Cited by 48 publications

References 230 publications

Deciphering the roles of FOXO1 in human neoplasms

Deciphering the roles of FOXO1 in human neoplasms

Enhanced Stabilization of MCL1 by the Human T-Cell Leukemia Virus Type 1 bZIP Factor Is Modulated by Blocking the Recruitment of Cullin 1 to the SCF Complex

A forceful connection: mechanoregulation of oncogenic YAP

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