Effects of BP-14, a novel cyclin-dependent kinase inhibitor, on anaplastic thyroid cancer cells

Allegri, Lorenzo; Baldan, Federica; Mio, Catia; Puppin, Cinzia; Russo, Diego; Kryštof, Vladimı́r; Damante, Giuseppe

doi:10.3892/or.2016.4614

Cited by 16 publications

(9 citation statements)

References 31 publications

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“…Several investigations were conducted to determine the relationship between drugs and some of them revealed crucial information about their behavior in combination. In this context, Allegri et al have shown a synergistic effect between a CDK inhibitor (BP-14) and a mTOR inhibitor (Everolimus) by demonstrating loss of cell viability and down-regulation of EMT-related genes [ 93 ]. Combination of the NF-κB inhibitor (Quinacrine) and Sorafenib showed improved survival in an orthotopic mouse model in comparison to vehicle-treated and Doxorubicin-treated mice [ 94 ].…”

Section: Promising Therapeutic Optionsmentioning

confidence: 99%

Therapeutic advances in anaplastic thyroid cancer: a current perspective

Saini¹,

Tulla²,

Maker³

et al. 2018

Mol Cancer

164

154

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Thyroid cancer incidence is increasing at an alarming rate, almost tripling every decade. In 2017, it was the fifth most common cancer in women. Although the majority of thyroid tumors are curable, about 2–3% of thyroid cancers are refractory to standard treatments. These undifferentiated, highly aggressive and mostly chemo-resistant tumors are phenotypically-termed anaplastic thyroid cancer (ATC). ATCs are resistant to standard therapies and are extremely difficult to manage. In this review, we provide the information related to current and recently emerged first-line systemic therapy (Dabrafenib and Trametinib) along with promising therapeutics which are in clinical trials and may be incorporated into clinical practice in the future. Different categories of promising therapeutics such as Aurora kinase inhibitors, multi-kinase inhibitors, epigenetic modulators, gene therapy using oncolytic viruses, apoptosis-inducing agents, and immunotherapy are reviewed. Combination treatment options that showed synergistic and antagonistic effects are also discussed. We highlight ongoing clinical trials in ATC and discuss how personalized medicine is crucial to design the second line of treatment. Besides using conventional combination therapy, embracing a personalized approach based on advanced genomics and proteomics assessment will be crucial to developing a tailored treatment plan to improve the chances of clinical success.

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Section: Promising Therapeutic Optionsmentioning

confidence: 99%

Therapeutic advances in anaplastic thyroid cancer: a current perspective

Saini¹,

Tulla²,

Maker³

et al. 2018

Mol Cancer

164

154

View full text Add to dashboard Cite

show abstract

“…In previous studies, we and others have already shown that the use of compounds extracted from plants is potentially useful in counteracting the growth of ATC cells in preclinical experimental models [ 20 , 21 , 22 , 40 , 41 ]. In particular, we demonstrated that DHT, a lipophilic abietane diterpene compound extracted from the dried root of Salvia miltiorrhiza , has an antitumor action in ATC cell lines, and this action is in part mediated by the regulation of the HuR-MAD2 axis known to be involved in the proliferation, survival and aggressiveness of this tumor [ 42 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

“…The clonogenic ability of the SW1736, 8505C, SW1736-PTX and 8505C-PTX cells was evaluated using a soft agar assay, as previously described [ 40 ]. Briefly, after 48 h of treatment, cells were collected, and 1 × 10 4 cells were suspended in 4 mL complete medium containing 0.25% agarose (Sigma-Aldrich), then seeded to the top of a 1% agarose complete medium layer in 6-cm plates.…”

Section: Methodsmentioning

confidence: 99%

Effects of Dihydrotanshinone I on Proliferation and Invasiveness of Paclitaxel-Resistant Anaplastic Thyroid Cancer Cells

Allegri

Capriglione

Maggisano

et al. 2021

IJMS

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ATC is a very rare, but extremely aggressive form of thyroid malignancy, responsible for the highest mortality rate registered for thyroid cancer. In patients without known genetic aberrations, the current treatment is still represented by palliative surgery and systemic mono- or combined chemotherapy, which is often not fully effective for the appearance of drug resistance. Comprehension of the mechanisms involved in the development of the resistance is therefore an urgent issue to suggest novel therapeutic approaches for this very aggressive malignancy. In this study, we created a model of anaplastic thyroid cancer (ATC) cells resistant to paclitaxel and investigated the characteristics of these cells by analyzing the profile of gene expression and comparing it with that of paclitaxel-sensitive original ATC cell lines. In addition, we evaluated the effects of Dihydrotanshinone I (DHT) on the viability and invasiveness of paclitaxel-resistant cells. ATC paclitaxel-resistant cells highlighted an overexpression of ABCB1 and a hyper-activation of the NF-κB compared to sensitive cells. DHT treatment resulted in a reduction of viability and clonogenic ability of resistant cells. Moreover, DHT induces a decrement of NF-κB activity in SW1736-PTX and 8505C-PTX cells. In conclusion, to the best of our knowledge, the results of the present study are the first to demonstrate the antitumor effects of DHT on ATC cells resistant to Paclitaxel in vitro.

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“…Since SCC-25 cells are capable of only limited proliferation in semisolid medium, the clonogenic activity of this cell line was evaluated by colony forming assay as previously described. 19 Cells were treated with vehicle (0.002% DMSO), JQ1 250 nmol/L, IBET-151 2 μmol/L, IBET-762 2 μmol/L for 72 hours. Treated SCC-25 cells were then seeded onto 10-cm plates.…”

Section: Colonyformingassaymentioning

confidence: 99%

Biological and molecular effects of bromodomain and extra‐terminal (BET) inhibitors JQ1, IBET‐151, and IBET‐762 in OSCC cells

Baldan

Allegri

Lazarević

et al. 2019

J Oral Pathology Medicine

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Background Despite improvements in oral squamous cell carcinoma (OSCC) management, survival rates remain relatively low and novel anti‐neoplastic agents are needed. Bromodomain and extra‐terminal (BET) inhibitors proved to be promising agents for cancer treatment. We investigated the effects of three BET inhibitors (JQ1, IBET‐151, IBET‐762) on SCC‐25 cell line and primary oral cancer cell culture. Methods Cell viability was evaluated by MTT. Protein levels of MCM5 and cleaved‐PARP were estimated by Western blot. Clonogenic and migratory abilities were determined by colony forming and scratch assays. BET inhibitors effects on mRNA levels of E‐Cadherin, Vimentin, SNAI1, SNAI2, CLU, SERPINI1, MCM5, c‐Myc, E2F, IL7R, and PPARg were analyzed by qPCR. Results BET inhibitors significantly reduced oral cancer cell viability. JQ1 showed the greatest effect reducing cell viability to 10%, both in SCC‐25 and primary OSCC cultures (P < 0.001), compared to control cells. Cells treated with BET inhibitors displayed a reduction to 50% in colony forming capacity compared to control cells (P < 0.0001) and the colonies were smaller; they also had a 50%‐60% reduction in migratory capacity (P < 0.05) compared to untreated cells. BET inhibitors had a significant impact on genes related to epithelial to mesenchymal transition and other cancer cell markers, notably on MCM5, a gene related to cell cycle control. Conclusions BET inhibitors induce both OSCC cell death and reduction of tumor aggressiveness. Molecular mechanisms of BET inhibition involve among others, MCM5 downregulation. Importantly, this study demonstrates for the first time the anti‐tumoral effect of IBET‐151 and IBET‐762 in oral cancer.

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Effects of BP-14, a novel cyclin-dependent kinase inhibitor, on anaplastic thyroid cancer cells

Cited by 16 publications

References 31 publications

Therapeutic advances in anaplastic thyroid cancer: a current perspective

Therapeutic advances in anaplastic thyroid cancer: a current perspective

Effects of Dihydrotanshinone I on Proliferation and Invasiveness of Paclitaxel-Resistant Anaplastic Thyroid Cancer Cells

Biological and molecular effects of bromodomain and extra‐terminal (BET) inhibitors JQ1, IBET‐151, and IBET‐762 in OSCC cells

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