Treatment with Biologicals in Rheumatoid Arthritis: An Overview

Rein, Philipp; Mueller, Ruediger B

doi:10.1007/s40744-017-0073-3

Cited by 132 publications

(101 citation statements)

References 106 publications

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“…Another compound identified by in‐cell WB and PI staining in Tam‐Res MCF‐7 cells that reduces ERα levels and inhibit cell proliferation is methotrexate (Abitrexate®), an inhibitor of the dihydrofolate reductase (DHFR) used to treat different kind of cancers (Vander Heiden, ) and autoimmune diseases (i.e., rheumatoid arthritis) (Rein & Mueller, ). Treatment of regular and Tam‐Res MCF‐7 with MTX results in a significant reduction in ERα content.…”

Section: Discussionmentioning

confidence: 99%

A high throughput method to study the physiology of E2:ERα signaling in breast cancer cells

Leone

Busonero

Acconcia

2017

Journal Cellular Physiology

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17β-estradiol (E2) regulates diverse physiological effects including cell proliferation through the estrogen receptor α (ERα), which as a transcription factor drives gene transcription and as an extra-nuclear localized receptor triggers the membrane-dependent activation of diverse kinase cascades. E2 also modifies ERα intracellular levels via diverse intracellular mechanisms. In this way, the E2-acivated ERα integrates signaling cascades with the modulation of receptor intracellular concentration and with the induction of DNA synthesis and ultimately drives cell proliferation. In turn, E2 signaling deregulation can cause many diseases including breast cancer (BC). Recently, we performed a Western blotting (WB)-based screen to identify novel pathways affecting ERα intracellular levels and BC cell proliferation. However, because WB lacks high throughput potential, a high-content method to detect all aspects of E2:ERα signaling (nuclear and extra-nuclear receptor activity, ERα levels, E2-induced DNA synthesis) is desirable. Here, we set up a rapid way to measure E2:ERα signaling in 96-well plate format. To demonstrate its robustness, we also challenged 4OH-tamoxifen resistant (Tam-Res) BC cells with a library of anti-cancer drugs and identified methotrexate (MTX) as a molecule inducing ERα degradation and preventing BC cell proliferation. Overall, our research provides a high-content technique to study the physiology of E2:ERα signaling in cells and further suggests a possible anti-ERα and anti-proliferative use for MTX in Tam-Res BCs.

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Section: Discussionmentioning

confidence: 99%

A high throughput method to study the physiology of E2:ERα signaling in breast cancer cells

Leone

Busonero

Acconcia

2017

Journal Cellular Physiology

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“…Nonetheless, biologics pose the problem of serious side effects, such as increased risk of infections. Other common side effects include neurologic diseases like multiple sclerosis and lymphoma [27-29]. …”

Section: Newer Medicationsmentioning

confidence: 99%

Rheumatoid Arthritis: A Brief Overview of the Treatment

et al. 2018

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Rheumatoid arthritis (RA) is a chronic, inflammatory, systemic autoimmune disease, affecting the joints with varying severity among patients. The risk factors include age, gender, genetics, and environmental exposure (cigarette smoking, air pollutants, and occupational). Many complications can follow, such as permanent joint damage requiring arthroplasty, rheumatoid vasculitis, and Felty syndrome requiring splenectomy if it remains unaddressed. As there is no cure for RA, the treatment goals are to reduce the pain and stop/slow further damage. Here, we present a brief summary of various past and present treatment modalities to address the complications associated with RA.

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“…An increasing number of studies are identifying a correlation between the cytokine networks and the RA pathogenesis . At present, tremendous achievement has been seen in developing effective treatment of RA, in which suppressing the inflammatory responses is the most effect method . However, further studies are necessary to discover the mechanism in inflammatory responses of RA .…”

Section: Introductionmentioning

confidence: 99%

“…7,8 At present, tremendous achievement has been seen in developing effective treatment of RA, in which suppressing the inflammatory responses is the most effect method. 5,9,10 However, further studies are necessary to discover the mechanism in inflammatory responses of RA. 11 Long non-coding RNAs (lncRNAs), transcripts in length longer than 200 nc, show the crucial role in inflammation.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MEG3 inhibits rheumatoid arthritis through miR‐141 and inactivation of AKT/mTOR signalling pathway

Liu

Meng

et al. 2019

J Cellular Molecular Medi

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Rheumatoid arthritis (RA) is a chronic inflammation mediated by autoimmune responses. MEG3, a kind of long noncoding RNA (lncRNA), participates in cell proliferation in cancer tissues. However, the correlation between MEG3 and RA is yet unclear. Therefore, to clarify how MEG3 works in RA, we performed a series of experiments using RA samples. We found that MEG3 was downregulated in the fibroblast‐like synoviocytes of RA patients (RA‐FLS), in comparison with healthy subjects. MEG3 was also down‐regulated evidently in lipopolysaccharide (LPS)‐treated chondrocyte. As part of our experiments, MEG3 was overexpressed in chondrocyte by transfection with lentivirus containing sequences encoding MEG3. In addition, in presence of LPS, reductions were identified not only in the cell proliferation, but also in the generation of interleukin‐23 (IL‐23), which, however were reversed in the lentivirus (containing MEG3‐encoding sequences)‐transfected chondrocytes. Up‐regulated MEG3 resulted in an increase the level of Ki67. Moreover, MEG3 was negatively correlated with miR‐141, and miR‐141 was up‐regulated in LPS‐treated chondrocyte. Inhibitory effects of MEG3 overexpression, mentioned above, were partially abolished by overexpressed miR‐141. Further, animal experiment also showed the inhibitory effect of MEG3 in overexpression on the AKT/mTOR signaling pathway. In‐vivoexperiments also showed that cell proliferation was facilitated by MEG3 overexpression with inhibited inflammation. In summary, the protective role of MEG3 in RA was proved to be exerted by the increase in the rate of proliferation, which might correlate to the regulatory role of miR‐141 and AKT/mTOR signal pathway, suggesting that MEG3 holds great promise as a therapeutic strategy for RA.

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Treatment with Biologicals in Rheumatoid Arthritis: An Overview

Cited by 132 publications

References 106 publications

A high throughput method to study the physiology of E2:ERα signaling in breast cancer cells

A high throughput method to study the physiology of E2:ERα signaling in breast cancer cells

Rheumatoid Arthritis: A Brief Overview of the Treatment

LncRNA MEG3 inhibits rheumatoid arthritis through miR‐141 and inactivation of AKT/mTOR signalling pathway

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