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Molecular Target and Action Mechanism of Anti-cancer Agents 2.0
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Molecular Target and Action Mechanism of Anti-cancer Agents 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 15692

Special Issue Editor

Prof. Dr. Seok-Geun Lee

E-Mail Website
Guest Editor
Department of Biomedical Science and Technology, Bionanocomposite Research Center, Kyung Hee Univerisity, 26 Kyungheedae-ro, Seoul 02447, Republic of Korea
Interests: molecular genetics; cancer biology; cancer pharmacology; bioactive phytochemicals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The idea of precision oncology is no longer new, but recent advances in functional genomics and proteomics are changing the way physicians and scientists approach the diagnosis of cancer risk as well as treatment. Although precision medicine is not yet part of routine care for most cancer patients, increased knowledge of cancer diagnosis with more detailed stratification based on patients’ genetic changes helps to move the field of precision oncology forward. Of course, developing new anticancer agents targeting genetic changes is another important part of precision oncology. In this context, this Special Issue aims to cover all areas of molecular-mechanism-based research for anticancer therapy. It welcomes original research, review articles, and short communications on specific molecular mechanisms of any anticancer agents, including conventional chemotherapy, novel potential anticancer drug candidates, and their combinations with any other anticancer modalities.

Prof. Dr. Seok-Geun Lee
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • Conventional therapy
  • Targeted therapy
  • Immunotherapy
  • Chemoprevention
  • Molecular target
  • Molecular mechanism
  • Drug resistance
  • Combinatorial therapy

Published Papers (4 papers)

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Research

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19 pages, 3474 KiB  
Article
SIRT1/FOXO Signaling Pathway in Breast Cancer Progression and Metastasis
by Sayra Dilmac, Nilay Kuscu, Ayse Caner, Sendegul Yildirim, Burcak Yoldas, Ammad Ahmad Farooqi and Gamze Tanriover
Int. J. Mol. Sci. 2022, 23(18), 10227; https://doi.org/10.3390/ijms231810227 - 6 Sep 2022
Cited by 15 | Viewed by 2950
Abstract
Breast cancer is the second most common cancer in women. The roles of the SIRT and FoxO proteins in tumor progression are known, but their roles in metastasis have not yet been clearly elucidated. In our study, we investigated the roles of SIRT [...] Read more.
Breast cancer is the second most common cancer in women. The roles of the SIRT and FoxO proteins in tumor progression are known, but their roles in metastasis have not yet been clearly elucidated. In our study, we investigated the roles of SIRT and FoxO proteins their downstream pathways, proteins p21 and p53, in tumor progression and metastasis. We evaluated these proteins in vitro using metastatic 4TLM and 67NR cell lines, as well as their expression levels in tumor-bearing mice. In addition, the regulatory role of SIRT and FoxO proteins in different transduction cascades was examined by IPA core analysis, and clinicopathological evidence was investigated in the TCGA database. In primary tumors, the expression levels of SIRT1, p21, p53, E2F1 and FoxO proteins were higher in 67NR groups. In metastatic tissues, the expression levels of SIRT1, E2F1 and FoxO proteins were found to be enhanced, whereas the levels of p53 and p21 expression were noted to be reduced. IPA analysis also provided empirical evidence of the mechanistic involvement of SIRT and FoxO proteins in tumor progression and metastasis. In conclusion, SIRT1 was found to co-operate with FoxO proteins and to play a critical role in metastasis. Additional research is required to determine why overexpression of SIRT1 in metastatic tissues has oncogenic effects. Full article
(This article belongs to the Special Issue Molecular Target and Action Mechanism of Anti-cancer Agents 2.0)
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16 pages, 27598 KiB  
Article
Combined Treatment with Cryptocaryone and Ultraviolet C Promotes Antiproliferation and Apoptosis of Oral Cancer Cells
by Sheng-Chieh Wang, Hsun-Shuo Chang, Jen-Yang Tang, Ammad Ahmad Farooqi, Yun-Tzu Kuo, Yan-Der Hsuuw, Jai-Wei Lee and Hsueh-Wei Chang
Int. J. Mol. Sci. 2022, 23(6), 2981; https://doi.org/10.3390/ijms23062981 - 10 Mar 2022
Cited by 6 | Viewed by 1755
Abstract
Cryptocaryone (CPC) was previously reported as preferential for killing natural products in oral cancer cells. However, its radiosensitizing potential combined with ultraviolet C (UVC) cell killing of oral cancer cells remains unclear. This study evaluates the combined anti-proliferation effect and clarifies the mechanism [...] Read more.
Cryptocaryone (CPC) was previously reported as preferential for killing natural products in oral cancer cells. However, its radiosensitizing potential combined with ultraviolet C (UVC) cell killing of oral cancer cells remains unclear. This study evaluates the combined anti-proliferation effect and clarifies the mechanism of combined UVC/CPC effects on oral cancer cells. UVC/CPC shows higher anti-proliferation than individual and control treatments in a low cytotoxic environment on normal oral cells. Mechanistically, combined UVC/CPC generates high levels of reactive oxygen species and induces mitochondrial dysfunction by generating mitochondrial superoxide, increasing mitochondrial mass and causing the potential destruction of the mitochondrial membrane compared to individual treatments. Moreover, combined UVC/CPC causes higher G2/M arrest and triggers apoptosis, with greater evidence of cell cycle disturbance, annexin V, pancaspase, caspases 3/7 expression or activity in oral cancer cells than individual treatments. Western blotting further indicates that UVC/CPC induces overexpression for cleaved types of poly (ADP-ribose) polymerase and caspase 3 more than individual treatments. Additionally, UVC/CPC highly induces γH2AX and 8-hydroxy-2’-deoxyguanosine adducts as DNA damage in oral cancer cells. Taken together, CPC shows a radiosensitizing anti-proliferation effect on UVC irradiated oral cancer cells with combined effects through oxidative stress, apoptosis and DNA damage. Full article
(This article belongs to the Special Issue Molecular Target and Action Mechanism of Anti-cancer Agents 2.0)
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Review

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50 pages, 7226 KiB  
Review
Targeted Protein Degradation: Clinical Advances in the Field of Oncology
by Abdelrahman K. A. A. Salama, Marija V. Trkulja, Emilio Casanova and Iris Z. Uras
Int. J. Mol. Sci. 2022, 23(23), 15440; https://doi.org/10.3390/ijms232315440 - 6 Dec 2022
Cited by 10 | Viewed by 6798
Abstract
The field of targeted protein degradation (TPD) is a rapidly developing therapeutic modality with the promise to tame disease-relevant proteins in ways that are difficult or impossible to tackle with other strategies. While we move into the third decade of TPD, multiple degrader [...] Read more.
The field of targeted protein degradation (TPD) is a rapidly developing therapeutic modality with the promise to tame disease-relevant proteins in ways that are difficult or impossible to tackle with other strategies. While we move into the third decade of TPD, multiple degrader drugs have entered the stage of the clinic and many more are expected to follow. In this review, we provide an update on the most recent advances in the field of targeted degradation with insights into possible clinical implications for cancer prevention and treatment. Full article
(This article belongs to the Special Issue Molecular Target and Action Mechanism of Anti-cancer Agents 2.0)
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18 pages, 2175 KiB  
Review
Regulation of Cell Signaling Pathways and Non-Coding RNAs by Baicalein in Different Cancers
by Ammad Ahmad Farooqi, Gulnara Kapanova, Sundetgali Kalmakhanov, Gulnur Tanbayeva, Kairat S. Zhakipbekov, Venera S. Rakhmetova and Marat K. Syzdykbayev
Int. J. Mol. Sci. 2022, 23(15), 8377; https://doi.org/10.3390/ijms23158377 - 29 Jul 2022
Cited by 7 | Viewed by 2868
Abstract
Landmark discoveries in molecular oncology have provided a wide-angle overview of the heterogenous and therapeutically challenging nature of cancer. The power of modern ‘omics’ technologies has enabled researchers to deeply and comprehensively characterize molecular mechanisms underlying cellular functions. Interestingly, high-throughput technologies have opened [...] Read more.
Landmark discoveries in molecular oncology have provided a wide-angle overview of the heterogenous and therapeutically challenging nature of cancer. The power of modern ‘omics’ technologies has enabled researchers to deeply and comprehensively characterize molecular mechanisms underlying cellular functions. Interestingly, high-throughput technologies have opened new horizons for the design and scientific fool-proof evaluation of the pharmacological properties of targeted chemical compounds to tactfully control the activities of the oncogenic protein networks. Groundbreaking discoveries have galvanized the expansion of the repertoire of available pharmacopoeia to therapeutically target a myriad of deregulated oncogenic pathways. Natural product research has undergone substantial broadening, and many of the drugs which constitute the backbone of modern pharmaceuticals have been derived from the natural cornucopia. Baicalein has gradually gained attention because of its unique ability to target different oncogenic signal transduction cascades in various cancers. We have partitioned this review into different sub-sections to provide a broader snapshot of the oncogenic pathways regulated by baicalein. In this review, we summarize baicalein-mediated targeting of WNT/β-catenin, AKT/mTOR, JAK/STAT, MAPK, and NOTCH pathways. We also critically analyze how baicalein regulates non-coding RNAs (microRNAs and long non-coding RNAs) in different cancers. Finally, we conceptually interpret baicalein-mediated inhibition of primary and secondary growths in xenografted mice. Full article
(This article belongs to the Special Issue Molecular Target and Action Mechanism of Anti-cancer Agents 2.0)
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