Arsenic trioxide suppressed mantle cell lymphoma by downregulation of cyclin D1

Lo, Rico K.H.; Kwong, Yok–Lam

doi:10.1007/s00277-013-1866-2

Cited by 16 publications

(10 citation statements)

References 33 publications

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“…Moreover, combination of ATO and ATRA exerts a synergistic effect in inhibiting breast cancer cell proliferation as compared with ATO or ATRA alone. In addition to PIN1, ATO can degrade other oncogenic proteins including cyclin D1 and nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) ( Lo and Kwong, 2014 ; Piao et al, 2017 ). All these findings suggest that both ATRA and ATO are attractive PIN1-targeting therapeutic drugs in the treatment of cancers.…”

Section: Development Of Pin1 Inhibitors For Cancer Treatmentmentioning

confidence: 99%

PIN1 in Cell Cycle Control and Cancer

Cheng

Tse

2018

Front. Pharmacol.

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Cell cycle progression is tightly controlled by many cell cycle-regulatory proteins that are in turn regulated by a family of cyclin-dependent kinases (CDKs) through protein phosphorylation. The peptidyl-prolyl cis/trans isomerase PIN1 provides a further post-phosphorylation modification and functional regulation of these CDK-phosphorylated proteins. PIN1 specifically binds the phosphorylated serine or threonine residue preceding a proline (pSer/Thr-Pro) motif of its target proteins and catalyzes the cis/trans isomerization on the pSer/Thr-Pro peptide bonds. Through this phosphorylation-dependent prolyl isomerization, PIN1 fine-tunes the functions of various cell cycle-regulatory proteins including retinoblastoma protein (Rb), cyclin D1, cyclin E, p27, Cdc25C, and Wee1. In this review, we discussed the essential roles of PIN1 in regulating cell cycle progression through modulating the functions of these cell cycle-regulatory proteins. Furthermore, the mechanisms underlying PIN1 overexpression in cancers were also explored. Finally, we examined and summarized the therapeutic potential of PIN1 inhibitors in cancer therapy.

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Section: Development Of Pin1 Inhibitors For Cancer Treatmentmentioning

confidence: 99%

PIN1 in Cell Cycle Control and Cancer

Cheng

Tse

2018

Front. Pharmacol.

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“…Importantly, ATO represses mantle cell lymphoma (MCL) through the downregulation of cyclin D1. This finding suggests that ATO may be clinically helpful in MCL . Meanwhile, ATO can be considered as a promising treatment for the patients with relapsed or refractory malignant lymphoma .…”

Section: Trace Elements and Cancermentioning

confidence: 86%

“…74 Meanwhile, ATO can be considered as a promising treatment for the patients with relapsed or refractory malignant lymphoma. 73,74 It has been shown that ATO has antiproliferative and proapoptotic effects on pancreatic cancer cell lines. 75 Regardless of encouraging in vitro evidence, ATO has no activity in patients with pancreatic cancer refractory to gemcitabine.…”

Section: The Role Of As In Cancermentioning

confidence: 99%

The crosstalk between trace elements with DNA damage response, repair, and oxidative stress in cancer

Tehrani

Hosseini

Yousefi

et al. 2018

J of Cellular Biochemistry

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DNA damage response (DDR) is a regulatory system responsible for maintaining genome integrity and stability, which can sense and transduce DNA damage signals. The severity of damage appears to determine DDRs, which can include damage repair, cell‐cycle arrest, and apoptosis. Furthermore, defective components in DNA damage and repair machinery are an underlying cause for the development and progression of various types of cancers. Increasing evidence indicates that there is an association between trace elements and DDR/repair mechanisms. In fact, trace elements seem to affect mediators of DDR. Besides, it has been revealed that oxidative stress (OS) and trace elements are associated with cancer development. In this review, we discuss the role of some critical trace elements in the risk of cancer. In addition, we provide a brief introduction on DDR and OS in cancer. Finally, we will further review the interactions between some important trace elements including selenium, zinc, chromium, cadmium, and arsenic, and DDR, and OS in cancer.

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“…Arsenic trioxide (ATO), is a FDA approved drug used for the treatment of APL that is refractory to or relapsed after ATRA therapy. The anti-cancer effect of ATO mainly depends on its ability to induce ubiquitin-dependent proteasomal degradation of various oncogenic proteins, including promyelocytic leukemia-retinoic acid receptor-alpha (PML-RARA) in APL, cyclin D1 in mantle cell lymphoma, and nucleophosminanaplastic lymphoma kinase (NPM-ALK) in anaplastic large cell lymphoma (Shao et al, 1998;Lo and Kwong, 2014;Piao et al, 2017). Through the proteasome pathway, ATO has also been found to induce PIN1 degradation by directly binding to the PIN1 PPIase domain (Kozono et al, 2018).…”

Section: Pin1 and Atomentioning

confidence: 99%

Targeting PIN1 as a Therapeutic Approach for Hepatocellular Carcinoma

Cheng

Tse

2020

Front. Cell Dev. Biol.

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PIN1 is a peptidyl-prolyl cis/trans isomerase that specifically binds and catalyzes the cis/trans isomerization of the phosphorylated serine or threonine residue preceding a proline (pSer/Thr-Pro) motif of its interacting proteins. Through this phosphorylationdependent prolyl isomerization, PIN1 is involved in the regulation of various important cellular processes including cell cycle progression, cell proliferation, apoptosis and microRNAs biogenesis; hence its dysregulation contributes to malignant transformation. PIN1 is highly expressed in hepatocellular carcinoma (HCC). By fine-tuning the functions of its interacting proteins such as cyclin D1, x-protein of hepatitis B virus and exportin 5, PIN1 plays an important role in hepatocarcinogenesis. Growing evidence supports that targeting PIN1 is a potential therapeutic approach for HCC by inhibiting cell proliferation, inducing cellular apoptosis, and restoring microRNAs biogenesis. Novel formulation of PIN1 inhibitors that increases in vivo bioavailability of PIN1 inhibitors represents a promising future direction for the therapeutic strategy of HCC treatment. In this review, the mechanisms underlying PIN1 over-expression in HCC are explored. Furthermore, we also discuss the roles of PIN1 in HCC tumorigenesis and metastasis through its interaction with various phosphoproteins. Finally, recent progress in the therapeutic options targeting PIN1 for HCC treatment is examined and summarized.

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Arsenic trioxide suppressed mantle cell lymphoma by downregulation of cyclin D1

Cited by 16 publications

References 33 publications

PIN1 in Cell Cycle Control and Cancer

PIN1 in Cell Cycle Control and Cancer

The crosstalk between trace elements with DNA damage response, repair, and oxidative stress in cancer

Targeting PIN1 as a Therapeutic Approach for Hepatocellular Carcinoma

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