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Life
Special Issues
Cancer Treatment and Drug Resistance
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Cancer Treatment and Drug Resistance

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Pharmaceutical Science".

Deadline for manuscript submissions: closed (1 January 2023) | Viewed by 9164

Special Issue Editors

Dr. Hamid Maadi

E-Mail Website
Guest Editor
Department of Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB T6G 1Z2, Canada
Interests: cancer biology; targeted cancer therapy; cell stress response; gene therapy; cancer genetics; pediatric cancer; cancer immunotherapy
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Zhixiang Wang

E-Mail Website
Guest Editor
Signal Transduction Research Group, Department of Medical Genetics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada
Interests: receptor tyrosine kinases; EGFR; signal transduction; cancer therapy; breast cancer treatment; targeted therapy
Special Issues, Collections and Topics in MDPI journals
Dr. Yaghub Pazhang

E-Mail Website
Guest Editor
Department of Biology, Faculty of sciences, University of Urmia, Urmia, Iran
Interests: apoptosis; cancer therapy; cell signaling

Special Issue Information

Dear Colleagues,

The uncontrolled growth of cells inside a tissue can cause a group of diseases that are collectively called cancer. The six common properties of cancer cells as identified by Drs. Hanahan and Weinberg are “sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis”. Since the discovery of the disease, several treatment strategies have been introduced to cure or expand the lifespan of patients with cancer. Generally, cancer treatment strategies can be stratified into four types: 1) treatments based on the physical removal or destruction of tumor tissue (e.g., surgery, radiotherapy); 2) systemic chemotherapy which targets highly proliferative cells; 3) targeted therapy which targets survival factors of cancer cells; and 4) immunotherapy which boosts the patient’s immune system to fight against cancer. Treatment strategies are usually selected based on cancer type, patient age, and tumor stage. Although the cancer treatments have improved the survival rate of patients with cancer, some patients do not respond or become resistant to the treatments.   

There are complex connections between cancer cells and various signaling pathways involved in cancer initiation, progression, and metastasis. Our limited knowledge about these signaling pathways is a hurdle to the design of efficient treatment strategies to cure cancer patients or overcome drug resistance. Therefore, identifying the key components of such signaling pathways would help us to increase the efficiency of current treatments, design novel therapies, and ultimately reduce the cancer-related mortality.

This Special Issue will cover the recent progress in all areas related to cancer treatment and drug resistance.

Dr. Hamid Maadi
Prof. Dr. Zhixiang Wang
Dr. Yaghub Pazhang
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer treatment
  • drug resistance
  • cancer cell signaling
  • metastasis
  • apoptosis
  • cell cycle
  • novel therapies

Published Papers (5 papers)

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Research

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13 pages, 2522 KiB  
Article
Attenuation of Endoplasmic Reticulum Stress Enhances Carvacrol-Induced Apoptosis in Osteosarcoma Cell Lines
by Kuan-Wei Chiu, Hsuan-Ying Chen, Chiu-Liang Chen, Cheng-Pu Hsieh and Yi-Fu Huang
Life 2023, 13(3), 744; https://doi.org/10.3390/life13030744 - 09 Mar 2023
Cited by 2 | Viewed by 1373
Abstract
Carvacrol is a monoterpenoid phenol that has excellent antimicrobial, antiviral, and anti-inflammatory activities. It can also improve wound healing. However, few studies have explored its antitumor effect on osteosarcoma. In this report, we tried to determine the potential efficacy of carvacrol against osteosarcoma [...] Read more.
Carvacrol is a monoterpenoid phenol that has excellent antimicrobial, antiviral, and anti-inflammatory activities. It can also improve wound healing. However, few studies have explored its antitumor effect on osteosarcoma. In this report, we tried to determine the potential efficacy of carvacrol against osteosarcoma cell lines. Our data revealed that carvacrol exposure inhibited the proliferation of osteosarcoma HOS and U-2 OS cells. In addition, carvacrol exposure enhanced the levels of cleaved PARP and caspase 3 and increased annexin V-positive cells, indicating that carvacrol exposure triggers apoptosis in osteosarcoma cell lines. Furthermore, the levels of reactive oxygen species (ROS) were enhanced after carvacrol exposure and cotreatment with NAC, the ROS scavenger, decreased the levels of cleaved PARP and caspase 3, suggesting the involvement of ROS in carvacrol-induced apoptosis. Importantly, we found that carvacrol exposure triggered several protein expressions related to endoplasmic reticulum (ER) stress, including GRP78/Bip, IRE1a, PERK, and CHOP, in HOS and U-2 OS cells, indicating that carvacrol exposure could result in ER stress in these cell lines. Cotreatment with the ER stress inhibitor 4-PBA increased the levels of cleaved PARP and caspase 3 and further suppressed cellular proliferation in carvacrol-exposed osteosarcoma cell lines. Overall, the results indicate that induced ER stress can protect cells from apoptosis, but increased ROS contributes to apoptosis in carvacrol-treated cells. In this report, we first demonstrate the role of ER stress in carvacrol-induced apoptosis and suggest that ER stress could be targeted to enhance the antitumor activity of carvacrol in osteosarcoma cell lines. Full article
(This article belongs to the Special Issue Cancer Treatment and Drug Resistance)
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14 pages, 3021 KiB  
Article
Characterization of Stable Pyrazole Derivatives of Curcumin with Improved Cytotoxicity on Osteosarcoma Cell Lines
by Giordana Feriotto, Riccardo Rondanin, Paolo Marchetti, Federico Tagliati, Simone Beninati, Claudio Tabolacci, Elisa Grusi, Serena Aguzzi and Carlo Mischiati
Life 2023, 13(2), 431; https://doi.org/10.3390/life13020431 - 03 Feb 2023
Cited by 3 | Viewed by 1442
Abstract
Curcumin (CUR) is a natural molecule that is unstable due to the presence of a bis-ketone. To obtain more stable derivatives in biological fluids, the bis-ketone was replaced with pyrazole or O-substituted oximes. Their stability in solution was studied by UV–visible spectrophotometry. The [...] Read more.
Curcumin (CUR) is a natural molecule that is unstable due to the presence of a bis-ketone. To obtain more stable derivatives in biological fluids, the bis-ketone was replaced with pyrazole or O-substituted oximes. Their stability in solution was studied by UV–visible spectrophotometry. The effects on proliferation were studied by MTT assay and/or clonogenicity assay. Induction of apoptosis was evaluated by annexin V staining and Western blot analysis. The bioavailability was obtained from the analysis of the molecular chemical–physical characteristics. The replacement of the bis-ketone with a pyrazole ring or O-substituted oximes improved the stability of all the CUR-derivative molecules. These derivatives were more stable than CUR in solution and were generally cytotoxic on a panel of cancer cell lines tested, and they promoted caspase-dependent apoptosis. Derivative 1 was the most potent in the osteosarcoma (OS) lines. With respect to CUR, this derivative showed cytotoxicity at least three times higher in the MTT assay. In addition, in the clonogenic assay, 1 maintained the activity in conditions of long treatment presumably by virtue of its improved stability in biological fluids. Notably, 1 should have improved chemical–physical characteristics of bioavailability with respect to CUR, which should allow for reaching higher blood levels than those observed in the CUR trials. In conclusion, 1 should be considered in future clinical studies on the treatment of OS, either alone or in combination with other medications currently in use. Full article
(This article belongs to the Special Issue Cancer Treatment and Drug Resistance)
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12 pages, 1987 KiB  
Article
Suppression of SREBP-1 Expression by Simvastatin Decreases Visfatin-Induced Chemoresistance to Sunitinib in Human Renal Carcinoma 786-O Cells
by Te-Chuan Chen, Chen-Wei Huang, Chih-Yu Lo, Cheng-Nan Chen, Shun-Fu Chang and Yih-Yuan Chen
Life 2022, 12(11), 1890; https://doi.org/10.3390/life12111890 - 15 Nov 2022
Cited by 1 | Viewed by 1412
Abstract
The resistance of renal cell carcinoma (RCC) to sunitinib impedes the success of chemotherapy in cancer treatment. Although several sunitinib resistance mechanisms have been proposed, little is known concerning the impact of obesity and adipokines in RCC cells. The upregulation of sterol-regulatory element-binding [...] Read more.
The resistance of renal cell carcinoma (RCC) to sunitinib impedes the success of chemotherapy in cancer treatment. Although several sunitinib resistance mechanisms have been proposed, little is known concerning the impact of obesity and adipokines in RCC cells. The upregulation of sterol-regulatory element-binding protein-1 (SREBP-1) has been reported to modulate the progression of tumor cells. The present study investigated the effect of visfatin on sunitinib-induced cytotoxicity in RCC cells through SREBP-1 expression. We found that visfatin-induced Akt and p70S6K activation increased SREBP-1 expression in 786-O cells. The visfatin-induced SREBP-1 mRNA and protein levels were attenuated through the inactivation of Akt and p70S6K by pharmacological inhibitors. In addition, the SREBP-1 knockdown using siRNA enhanced the cytotoxic effects of sunitinib. Our results also revealed the roles of simvastatin in attenuating the effects of visfatin on 786-O cells by inhibiting the production of reactive oxygen species. In particular, simvastatin co-treatment increased the cell cytotoxicity of sunitinib in visfatin-treated 786-O cells, which were associated with down-regulation of SREBP-1 expression. Our results suggest an important role of SREBP-1 in visfatin-induced drug resistance of RCC cells to sunitinib. The cytotoxic mechanism of simvastatin on RCC cells may provide a new strategy to improve therapeutic outcomes for the RCC treatment. Full article
(This article belongs to the Special Issue Cancer Treatment and Drug Resistance)
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18 pages, 1896 KiB  
Article
Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors
by Sofija Jovanović Stojanov, Ana Kostić, Mila Ljujić, Ema Lupšić, Silvia Schenone, Milica Pešić and Jelena Dinić
Life 2022, 12(10), 1503; https://doi.org/10.3390/life12101503 - 27 Sep 2022
Cited by 5 | Viewed by 2111
Abstract
Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability [...] Read more.
Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability of two Src tyrosine kinase inhibitors, Si306 and its prodrug pro-Si306, to induce autophagy was evaluated in the human glioblastoma cell line U87 and its multidrug-resistant counterpart U87-TxR. Autophagy markers were assessed by flow cytometry, microscopy, and Western blot, and induction of autophagy by these compounds was demonstrated after 3 h as well as 48 h. The effects of Si306 and pro-Si306 on cell proliferation and cell death were examined in the presence or absence of autophagy inhibition by bafilomycin A1. Combined treatments of Si306 and pro-Si306 with bafilomycin A1 were synergistic in nature, and the inhibition of autophagy sensitized glioblastoma cells to Src tyrosine kinase inhibitors. Si306 and pro-Si306 more strongly inhibited cell proliferation and triggered necrosis in combination with bafilomycin A1. Our findings suggest that modulation of Si306- and pro-Si306-induced autophagy can be used to enhance the anticancer effects of these Src tyrosine kinase inhibitors and overcome the drug-resistant phenotype in glioblastoma cells. Full article
(This article belongs to the Special Issue Cancer Treatment and Drug Resistance)
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11 pages, 1087 KiB  
Review
The Immunotherapeutic Role of Type I and III Interferons in Melanoma and Non-Melanoma Skin Cancers
by Sydney A. Weir, Kailash KC, Shoaib Shoaib and Nabiha Yusuf
Life 2023, 13(6), 1310; https://doi.org/10.3390/life13061310 - 01 Jun 2023
Cited by 2 | Viewed by 1793
Abstract
Interferons (IFNs) have demonstrated therapeutic potential in various skin cancers, specifically squamous cell carcinoma (SCC), basal cell carcinoma (BCC), and melanoma. The precise mechanism through which type I IFNs exert their antitumor effects in skin cancers is still being studied. However, intralesional type [...] Read more.
Interferons (IFNs) have demonstrated therapeutic potential in various skin cancers, specifically squamous cell carcinoma (SCC), basal cell carcinoma (BCC), and melanoma. The precise mechanism through which type I IFNs exert their antitumor effects in skin cancers is still being studied. However, intralesional type I IFN can be used as an alternative to surgery for select patient populations, and high-dose systemic IFN therapy has been shown to be promising in patients with operable high-risk or metastatic melanoma. Despite the therapeutic potential of IFNs in skin cancer treatment, the toxicity profile often prevents the completion of treatment and further expansion of its clinical application. Type I and III IFNs use the same Janus Kinases (JAKs) for signal transduction, which are pathways initiated at a cell surface receptor that mediates the activation of target genes in the nucleus, based on this shared signaling pathway. Due to selective tumor targeting and the ability to generate both innate and adaptive immune responses, we concluded that type III IFNs have minimal side effects compared with established treatments due to selective tumor targeting. While IFN-λ, a type III IFN, shows therapeutic potential as stand-alone or in combination with another IFN, further studies need to be conducted to explore the therapeutic potential of IFN-λ in skin cancer and the underlying physiological roles and mechanisms of action. In this review, we evaluate whether treatment of skin cancer with type III IFN will have minimal side effects compared with established treatments. Full article
(This article belongs to the Special Issue Cancer Treatment and Drug Resistance)
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