Oral and IV Dosages of Doxorubicin-Methotrexate loaded-Nanoparticles Inhibit Progression of Oral Cancer by Down-Regulation of Matrix Methaloproteinase 2 Expression in Vivo

Abbasi, Mehran Mesgari; Jahanban‐Esfahlan, Rana; Amir, Mohammad; Seidi, Khaled; Hamishehkar, Hamed; Khiavi, Monir Moradzadeh

doi:10.7314/apjcp.2014.15.24.10705

Cited by 31 publications

(28 citation statements)

References 38 publications

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“…We have clearly demonstrated the importance of cortisol on oral cancer cells' ability to survive and combat the effectiveness of two (Abbasi et al, 2014). However, the current study is the first to investigate and demonstrate the effect of DOXO in vitro on several human OSCC cell lines, indicating its future potential for the treatment of OSCC.…”

Section: Discussionmentioning

confidence: 78%

Glucocorticoids reduce chemotherapeutic effectiveness on OSCC cells via glucose‐dependent mechanisms

Celentano

McCullough

Cirillo

2018

Journal Cellular Physiology

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Synthetic corticosteroids are routinely administered during the treatment of several diseases, including malignancies. However, recent evidence suggests that corticosteroids may have tumor‐promoting effects, particularly in epithelial neoplasms. Our aim was to assess the role of the recently characterized cancer‐associated glucocorticoid (GC) system in the resistance to chemotherapy of oral malignant keratinocytes. Human malignant oral keratinocyte cell lines H314/H357/H400/BICR16/BICR56 were tested with: two chemotherapeutic agents, doxorubicin (DOXO) and 5‐fluorouracil (5‐FU), as well as hydrocortisone (HC), adrenocorticotropic hormone (ACTH), 5‐pregnen‐3‐beta‐ol‐20‐one‐16‐alfa‐carbonitrile (PCN), and two glucose uptake inhibitors, Fasentin and WZB. Both DOXO and 5‐FU induced apoptosis in a dose‐dependent and time‐dependent manner. HC administration (100 nM) reduced the effectiveness of both chemotherapeutic agents to a variable extent in all 5 oral squamous cell carcinoma cell lines. ACTH also reduced the effectiveness of DOXO on 2 cell lines tested (H357 and BICR56). The glucose uptake inhibitors Fasentin and WZB were able to partially block the increased resistance to the cytotoxic drugs induced by HC. In summary, we have demonstrated, for the first time, the importance of cortisol on oral cancer cells ability to proliferate and combat the effectiveness of chemotherapeutic agents. This effect appears to be glucose dependent.

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Section: Discussionmentioning

confidence: 78%

Glucocorticoids reduce chemotherapeutic effectiveness on OSCC cells via glucose‐dependent mechanisms

Celentano

McCullough

Cirillo

2018

Journal Cellular Physiology

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“…In addition, UA inhibited the ability of Ca922 cells to invade Matrigel‐coated membranes in a concentration‐dependent manner (Figure C). Previous studies reported that the overexpression of matrix metalloproteinase (MMP)‐2 is associated with the regional relapse of OSCC, and its downregulation inhibited OSCC progression in a chemotherapeutic agent‐treated animal model . We assessed if UA suppressed MMP‐2 activity in the conditioned medium using gelatin zymography.…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies reported that the overexpression of matrix metalloproteinase (MMP)-2 is associated with the regional relapse of OSCC, and its downregulation inhibited OSCC progression in a chemotherapeutic agent-treated animal model. 30,31 We assessed if UA suppressed MMP-2 activity in the conditioned medium using gelatin zymography. As shown in Figure 3D, the proteolytic activity of MMP-2 was reduced after UA treatment for 36 hours.…”

Section: In Addition Ua Inhibited the Ability Of Ca922 Cells To Invadementioning

confidence: 99%

Ursolic acid induces apoptosis and autophagy in oral cancer cells

Lin

Chin

Lee

et al. 2019

Environmental Toxicology

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Oral squamous cell carcinoma (OSCC) is the fifth common cause of cancer mortality in Taiwan with high incidence and recurrence and needs new therapeutic strategies. In this study, ursolic acid (UA), a triterpenoid, was examined the antitumor potency in OSCC cells. Our results showed that UA inhibited the proliferation of OSCC cells in a dose‐ and time‐dependent manner in both Ca922 and SCC2095 oral cancer cells. UA induced caspase‐dependent apoptosis accompanied with the modulation of various biological biomarkers including downregulating Akt/mTOR/NF‐κB signaling, ERK, and p38. In addition, UA inhibited angiogenesis as evidenced by abrogation of migration/invasion and blocking MMP‐2 secretion in Ca922 cells. Interestingly, UA induced autophagy in OSCC cells, as manifested by LC3B‐II conversion and increased p62 expression and accumulation of autophagosomes. Inhibition by autophagy inhibitor enhanced UA‐mediated apoptosis in Ca922 cells. The experiment provides a rationale for using triterpenoid in the treatment of OSCC.

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“…Apoptosis and DNA damage was significantly increased in the dual-drug-loaded liposome group compared to other controls. Abbasi et al [53][54][55] examined stimuli-responsive cationic mesoporous silica NPs loaded with MTX and Dox on a 4-NQO-induced oral cavity SCC rat model. Both free and nanoforms of Dox combined with MTX were orally or IV administrated for 14 weeks.…”

Section: Doxorubicinmentioning

confidence: 99%

Nanomedicine, an emerging therapeutic strategy for oral cancer therapy

et al. 2018

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Oral cavity and oropharyngeal carcinomas (oral cancer) represents a significant cause of morbidity and mortality. Despite efforts in improving early diagnosis and treatment, the 5-year survival rate of advanced stage of the disease is less than 63%. The field of nanomedicine has offered promising diagnostic and therapeutic advances in cancer. Indeed, several platforms have been clinically approved for cancer therapy, while other promising systems are undergoing exploration in clinical trials. With its ability to deliver drugs, nucleic acids, and MRI contrast agents with high efficiency, nanomedicine platforms offer the potential to improve drug efficacy and tolerability. The aim of the present mini-review is to summarize the current preclinical status of nanotechnology systems for oral cancer therapy. The nanoplatforms for delivery of chemopreventive agents presented herein resulted in significantly higher anti-tumor activity than free forms of the drug, even against a chemo-resistant cell line. Impressive results have also been obtained using nanoparticles to deliver chemotherapeutics, resulting in reduced toxicity both in vitro and in vivo. Nanoparticles have also led to improvements in efficacy of photodynamic therapies through the development of targeted magnetic nanoparticles. Finally, gene therapy using nanoparticles demonstrated promising results specifically with regards to inhibition of gene expression. Of the few in vivo studies that have been reported, many of these used animal models with several limitations, which will be discussed herein. Lastly, we will discuss several future perspectives in oral cancer nanoparticle-based therapy and the development of appropriate animal models, distinguishing between oral cavity and oropharyngeal carcinoma.

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Oral and IV Dosages of Doxorubicin-Methotrexate loaded-Nanoparticles Inhibit Progression of Oral Cancer by Down-Regulation of Matrix Methaloproteinase 2 Expression in Vivo

Cited by 31 publications

References 38 publications

Glucocorticoids reduce chemotherapeutic effectiveness on OSCC cells via glucose‐dependent mechanisms

Glucocorticoids reduce chemotherapeutic effectiveness on OSCC cells via glucose‐dependent mechanisms

Ursolic acid induces apoptosis and autophagy in oral cancer cells

Nanomedicine, an emerging therapeutic strategy for oral cancer therapy

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