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Nutrition and Cancer: Recent Advances and Future Perspectives

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 (31 January 2022) | Viewed by 6291

Special Issue Editor


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Guest Editor
Department of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea
Interests: cancer; herbal medicine; herbal extracts; Korean medicine; natural product; cancer therapy; chemotherapy
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Special Issue Information

Dear Colleagues,

Nutrition plays a potential role in cancer, and the relationship between nutrients and cancer is important in studying the mechanisms of tumor growth, survival, and repression. Anticancer drugs play a major role in cancer therapy. However, this strategy has many side effects and the therapeutic obstacle of chemoresistance. Today, many nutrients are being increasingly suggested as effective anticancer agents for cancer therapy and prevention. Several exert powerful anticancer effects via cell-death-related mechanisms such as apoptosis, ER stress, autophagic cell death, necroptosis, endocytosis, cell cycle arrest, antiangiogenic effects, antimetastatic effects, and epigenetic modification. Furthermore, nutrients exert anticancer effects under normoxia and hypoxia and enhance anticancer effects via diverse mechanisms in various resistant models such as multidrug resistance (MDR), radioresistance and nutrient deprivation.

This Special Issue of IJMS, “Nutrition and Cancer”, will focus on the interplay between cell death and cell survival with nutrients in cancer. In this Special Issue, there has been particular interest in antitumor therapeutic strategies based on cell death, cell survival, cell signaling, molecular mechanisms, and chemoresistance.

Prof. Dr. Seong-Gyu Ko
Guest Editor

Manuscript Submission Information

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Keywords

  • nutrient deprivation
  • hypoxia
  • metabolic stress
  • cell signaling
  • cell death
  • apoptosis
  • cancer
  • autophagy
  • epigenetics
  • chemoresistance

Published Papers (2 papers)

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Research

18 pages, 6243 KiB  
Article
JI017, a Complex Herbal Medication, Induces Apoptosis via the Nox4–PERK–CHOP Axis in Ovarian Cancer Cells
by Taewoo Kim and Seong-Gyu Ko
Int. J. Mol. Sci. 2021, 22(22), 12264; https://doi.org/10.3390/ijms222212264 - 12 Nov 2021
Cited by 6 | Viewed by 2567
Abstract
Many anti-cancer drugs, including paclitaxel and etoposide, have originated and been developed from natural products, and traditional herbal medicines have fewer adverse effects and lesser toxicity than anti-tumor reagents. Therefore, we developed a novel complex herbal medicine, JI017, which mediates endoplasmic reticulum (ER) [...] Read more.
Many anti-cancer drugs, including paclitaxel and etoposide, have originated and been developed from natural products, and traditional herbal medicines have fewer adverse effects and lesser toxicity than anti-tumor reagents. Therefore, we developed a novel complex herbal medicine, JI017, which mediates endoplasmic reticulum (ER) stress and apoptosis through the Nox4–PERK–CHOP signaling pathway in ovarian cancer cells. JI017 treatment increases the expression of GRP78, ATF4, and CHOP and the phosphorylation of PERK and eIF2α via the upregulation of Nox4. Furthermore, it increases the release of intracellular reactive oxygen species (ROS), the production of intracellular Ca2+, and the activation of exosomal GRP78 and cell lysate GRP78. Combination treatment using the sarco/endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin (TG) and JI017 reportedly induces increased ER stress and cell death in comparison to the control; however, knockdown experiments of PERK and CHOP indicated suppressed apoptosis and ER stress in JI017-treated ovarian cancer cells. Furthermore, targeting Nox4 using specific siRNA and pharmacological ROS inhibitors, including N-acetylcystein and diphenylene iodonium, blocked apoptosis and ER stress in JI017-treated ovarian cancer cells. In the radioresistant ovarian cancer model, when compared to JI017 alone, JI017 co-treatment with radiation induced greater cell death and resulted in overcoming radioresistance by inhibiting epithelial–mesenchymal-transition-related phenomena such as the reduction of E-cadherin and the increase of N-cadherin, vimentin, Slug, and Snail. These findings suggest that JI017 is a powerful anti-cancer drug for ovarian cancer treatment and that its combination treatment with radiation may be a novel therapeutic strategy for radioresistant ovarian cancer. Full article
(This article belongs to the Special Issue Nutrition and Cancer: Recent Advances and Future Perspectives)
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17 pages, 3672 KiB  
Article
Synergistic Antitumor Activity of SH003 and Docetaxel via EGFR Signaling Inhibition in Non-Small Cell Lung Cancer
by Mi-So Jeong, Kang-Wook Lee, Yu-Jeong Choi, Yun-Gyeong Kim, Hyun-Ha Hwang, Seo-Yeon Lee, Se-Eun Jung, Sun-Ah Park, Jin-Hee Lee, Yong-Joon Joo, Sung-Gook Cho and Seong-Gyu Ko
Int. J. Mol. Sci. 2021, 22(16), 8405; https://doi.org/10.3390/ijms22168405 - 05 Aug 2021
Cited by 15 | Viewed by 2889
Abstract
Epidermal growth factor receptor (EGFR) is overexpressed in lung cancer patients. Despite treatment with various EGFR tyrosine kinase inhibitors, recurrence and metastasis of lung cancer are inevitable. Docetaxel (DTX) is an effective conventional drug that is used to treat various cancers. Several researchers [...] Read more.
Epidermal growth factor receptor (EGFR) is overexpressed in lung cancer patients. Despite treatment with various EGFR tyrosine kinase inhibitors, recurrence and metastasis of lung cancer are inevitable. Docetaxel (DTX) is an effective conventional drug that is used to treat various cancers. Several researchers have studied the use of traditional herbal medicine in combination with docetaxel, to improve lung cancer treatment. SH003, a novel herbal mixture, exerts anticancer effects in different cancer cell types. Here, we aimed to investigate the apoptotic and anticancer effects of SH003 in combination with DTX, in human non-small-cell lung cancer (NSCLC). SH003, with DTX, induced apoptotic cell death, with increased expression of cleaved caspases and cleaved poly (ADP-ribose) polymerase in NSCLC cells. Moreover, SH003 and DTX induced the apoptosis of H460 cells via the suppression of the EGFR and signal transducer and activator of transcription 3 (STAT3) signaling pathways. In H460 tumor xenograft models, the administration of SH003 or docetaxel alone diminished tumor growth, and their combination effectively killed cancer cells, with increased expression of apoptotic markers and decreased expression of p-EGFR and p-STAT3. Collectively, the combination of SH003 and DTX may be a novel anticancer strategy to overcome the challenges that are associated with conventional lung cancer therapy. Full article
(This article belongs to the Special Issue Nutrition and Cancer: Recent Advances and Future Perspectives)
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