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Tumor Microenvironment Regulation and Anti-cancer Natural Products

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 30163

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Special Issue Editor

Dr. Chung-Jung Liu

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Guest Editor

1. Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
2. Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan
Interests: cancer; signaling pathways

Special Issue Information

Dear Colleagues,

Accumulation of genetic and epigenetic changes in cells finally induces the formation of cancer cells. These changes may be induced and influenced by the tumor microenvironment (TME). The TME plays an important role in tumor growth, angiogenesis, and metastasis. The occurrence of inflammation and recruitment of mesenchymal stem cells, fibroblasts, immune cells, etc. are shown to provide a favorable environment for tumor progression. Tumor cells interact with these cells, and/or their surrounding tissues become important issues for the maturation of the tumor environment and malignant tumors. Transfer of mitochondria and metabolites between tumor cells and surrounding stromal cells promotes the altered tumor metabolism, disease progression, and altered treatment responses in tumors. Additionally, microbiota that influence inflammation and immunity are reported to regulate the TME and the response to various types of cancer chemotherapy by affecting their mechanism of action and toxicity. Natural compounds against cancer cells and their microenvironment are considered an auxiliary treatment.

So far, the mechanisms behind microenvironment-mediated tumor progression have been largely unknown. Recently, more information regarding their potential role in tumor development is becoming available. Therefore, understanding and recreating a signaling environment to control tumor cell development is a critical stepping stone of translation medicine research in cancer treatment.

We are soliciting papers regarding tumor microenvironment regulation in human tumor development and natural components (with defined molecular compound) against cancer. We are particularly interested in articles reporting the relevance of microenvironment-regulating factors, candidate genes, stem cells, fibroblast and immune cells, etc. for tumor malignancy and natural products for cancer therapies. We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the underlying molecular mechanism issue, the development of potential anticancer component discovery, and strategies to treat cancer diseases.

Potential topics include but are not limited to:

Microbiota in tumor progression and cancer therapy
Role of mesenchymal stem cells, fibroblasts, immune cells, etc. in the regulation of tumor progression (growth, invasion, angiogenesis, drug resistance, etc.)
Modulation of the extracellular matrix and tumor progression;
Mitochondria-altered tumor metabolism and cancer progression;
Networks of cytokines/chemokines, growth factors and microRNA in the regulation of microenvironment-mediated tumorigenicity;
Cell signaling networks between altered microenvironment and tumor cells;
Cancer stem cell identifying, characterizing, tracking, targeting, or modeling;
Genetic and epigenetic changes in tumor cells, mesenchymal stem cells, fibroblast and immune cells, etc. leading to cancer progression;
Identification of molecular targets; innovative and ground-breaking strategies for cancer;
Potential anticancer natural component discovery and therapy.

Dr. Chung-Jung Liu
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. Biomedicines 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.

Published Papers (11 papers)

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Research

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10 pages, 2827 KiB

Open AccessArticle

Emodin Ameliorates the Efficacy of Carfilzomib in Multiple Myeloma Cells via Apoptosis and Autophagy

by Chin-Mu Hsu, Chia-Hung Yen, Shu-Chen Wang, Yi-Chang Liu, Chien-Tzu Huang, Min-Hong Wang, Tzer-Ming Chuang, Ya-Lun Ke, Tsung-Jang Yeh, Yuh-Ching Gau, Jeng-Shiun Du, Hui-Ching Wang, Shih-Feng Cho, Yuhsin Tsai, Chi-En Hsiao, Samuel Yien Hsiao and Hui-Hua Hsiao

Biomedicines 2022, 10(7), 1638; https://doi.org/10.3390/biomedicines10071638 - 08 Jul 2022

Cited by 6 | Viewed by 1952

Abstract

Background: Carfilzomib, the proteasome inhibitor, can increase the overall survival rate of multiple myeloma (MM) patients undergoing targeted therapy. However, relapse and toxicity present great challenges for such treatment, so an urgent need for effective combination therapy is necessary. Emodin is a natural chemical compound that inhibits the proliferation of various cancers and can effectively combine with other treatments. In this study, we evaluated the sensitizing effect of emodin combined with carfilzomib on MM cells. Methods: The cells were treated with emodin, carfilzomib, and a combination of drugs to determine their effects on cell proliferation and viability. The cell cycle distribution and reactive oxygen species (ROS) expression were measured by flow cytometry. The level of RNA and protein were analyzed through real-time qPCR and immunoblotting. Results: Emodin acted synergistically with carfilzomib to reduce the proliferation and viability of MM cell lines in vitro. Furthermore, the combination of emodin and carfilzomib increased ROS production, inducing apoptosis and autophagy pathways via caspase-3, PARP, p62, and LC3B. Conclusions: These results provide a molecular target for combination therapy in MM patients. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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18 pages, 3616 KiB

Open AccessEditor’s ChoiceArticle

Isoliquiritigenin Inhibits Gastric Cancer Stemness, Modulates Tumor Microenvironment, and Suppresses Tumor Growth through Glucose-Regulated Protein 78 Downregulation

by Chien-Hsing Lee, Hsin-Yi Tsai, Chun-Lin Chen, Jen-Lung Chen, Chao-Chun Lu, Yi-Ping Fang, Deng-Chyang Wu, Yaw-Bin Huang and Ming-Wei Lin

Biomedicines 2022, 10(6), 1350; https://doi.org/10.3390/biomedicines10061350 - 08 Jun 2022

Cited by 17 | Viewed by 2985

Abstract

Chemotherapy is the treatment of choice for gastric cancer; however, the currently available therapeutic drugs for treatment have limited efficacy. Cancer stemness and the tumor microenvironment may play crucial roles in tumor growth and chemoresistance. Glucose-regulated protein 78 (GRP78) is an endoplasmic reticulum chaperone facilitating protein folding and cell homeostasis during stress and may participate in chemoresistance. Isoliquiritigenin (ISL) is a bioactive flavonoid found in licorice. In this study, we demonstrated the role of GRP78 in gastric cancer stemness and evaluated GRP78-mediated stemness inhibition, tumor microenvironment regulation, and chemosensitivity promotion by ISL. ISL not only suppressed GRP78-mediated gastric cancer stem cell–like characteristics, stemness-related protein expression, and cancer-associated fibroblast activation but also gastric tumor growth in xenograft animal studies. The findings indicated that ISL is a promising candidate for clinical use in combination chemotherapy. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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15 pages, 4334 KiB

Open AccessArticle

Carbonic Anhydrase VIII (CAVIII) Gene Mediated Colorectal Cancer Growth and Angiogenesis through Mediated miRNA 16-5p

by Mingli Hsieh, Pei-Ju Huang, Pei-Yu Chou, Shih-Wei Wang, Hsi-Chi Lu, Wei-Wen Su, Yuan-Chiang Chung and Min-Huan Wu

Biomedicines 2022, 10(5), 1030; https://doi.org/10.3390/biomedicines10051030 - 29 Apr 2022

Cited by 2 | Viewed by 1670

Abstract

Carbonic anhydrase VIII (CAVIII) is a member of the CA family, while CA8 is the oncogene. Here we observed increased expression of CAVIII with high expression in colorectal cancer tissues. CAVIII is also expressed in more aggressive types of human colorectal cancer cells. Upregulated CAVIII expression in SW480 cell lines increased vascular endothelial growth factor (VEGF) and reduced miRNA16-5p. Conversely, knockdown of the CAVIII results in VEGF decline by up-regulated miRNA16-5p. Moreover, the collection of different grades of CAVIII expression CRC cells supernatant co-culture with endothelial progenitor cells (EPCs) promotes the ability of tube formation in soft agar and migration in the Transwell experiment, indicating that CAVIII might facilitate cancer-cell-released VEGF via the inhibition of miRNA16-5p signaling. Furthermore, in the xenograft tumor angiogenesis model, knockdown of CAVIII significantly reduced tumor growth and tumor-associated angiogenesis. Taken together, our results prove that the CAVIII/miR-16-5p signaling pathway might function as a metastasis suppressor in CRC. Targeting CAVIII/miR-16-5p may provide a strategy for blocking its metastasis. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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19 pages, 7653 KiB

Open AccessArticle

Phytochemically Derived Zingerone Nanoparticles Inhibit Cell Proliferation, Invasion and Metastasis in Human Oral Squamous Cell Carcinoma

by Cheng-Mei Yang, Tian-Huei Chu, Kuo-Wang Tsai, Shuchen Hsieh and Mei-Lang Kung

Biomedicines 2022, 10(2), 320; https://doi.org/10.3390/biomedicines10020320 - 29 Jan 2022

Cited by 7 | Viewed by 2611

Abstract

Due to its aggressiveness and high mortality rate, oral cancer still represents a tough challenge for current cancer therapeutics. Similar to other carcinomas, cancerous invasion and metastasis are the most important prognostic factors and the main obstacles to therapy for human oral squamous cell carcinoma (OSCC). Fortunately, with the rise of the nanotechnical era and innovative nanomaterial fabrication, nanomaterials are widely used in biomedicine, cancer therapeutics, and chemoprevention. Recently, phytochemical substances have attracted increasing interest as adjuvants to conventional cancer therapy. The ginger phenolic compound zingerone, a multitarget pharmacological and bioactive phytochemical, possesses potent anti-inflammatory, antioxidant, and anticancer activities. In our previous study, we generated phytochemically derived zingerone nanoparticles (NPs), and documented their superior antitumorigenic effect on human hepatoma cells. In the present study, we further investigated the effects of zingerone NPs on inhibiting the invasiveness and metastasis of human OSCC cell lines. Zingerone NPs elicited significant cytotoxicity in three OSCC cell lines compared to zingerone. Moreover, the lower dose of zingerone NPs (25 µM) markedly inhibited colony formation and colony survival by at least five-fold compared to zingerone treatment. Additionally, zingerone NPs significantly attenuated cell motility and invasiveness. In terms of the signaling mechanism, we determined that the zingerone NP-mediated downregulation of Akt signaling played an important role in the inhibition of cell viability and cell motility. Zingerone NPs inhibited matrix metalloproteinase (MMP) activity, which was highly correlated with the attenuation of cell migration and cell invasion. By further detecting the roles of zingerone NPs in epithelial–mesenchymal transition (EMT), we observed that zingerone NPs substantially altered the levels of EMT-related markers by decreasing the levels of the mesenchymal markers, N-cadherin and vimentin, rather than the epithelial proteins, ZO-1 and E-cadherin, compared with zingerone. In conclusion, as novel and efficient phytochemically derived nanoparticles, zingerone NPs may serve as a potent adjuvant to protect against cell invasion and metastasis, which will provide a beneficial strategy for future applications in chemoprevention and conventional therapeutics in OSCC treatment. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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12 pages, 25500 KiB

Open AccessArticle

Magnolol Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells through JNK1/2 and p38 Pathways

by Yi-Tzu Chen, Chiao-Wen Lin, Chun-Wen Su, Wei-En Yang, Chun-Yi Chuang, Shih-Chi Su, Ming-Ju Hsieh and Shun-Fa Yang

Biomedicines 2021, 9(10), 1295; https://doi.org/10.3390/biomedicines9101295 - 22 Sep 2021

Cited by 11 | Viewed by 2526

Abstract

Magnolol is a natural compound extracted from Chinese herbal medicine and can induce apoptosis in numerous types of cancer cells. However, the molecular mechanisms of magnolol in oral cancer are still unclear. In this study, we investigated the anti-cancer effects and underlying mechanisms of magnolol in human oral cancer cell lines. Our results exhibited that magnolol inhibited the cell proliferation via inducing the sub-G1 phase and cell apoptosis of HSC-3 and SCC-9 cells. The human apoptosis array and Western blot assay showed that magnolol increased the expression of cleaved caspase-3 proteins and heme oxygenase-1 (HO-1). Moreover, we proved that magnolol induces apoptosis in oral cancer cell lines via the c-Jun N-terminal kinase (JNK)1/2 and p38 pathways. Overall, the current study supports the role for magnolol as a therapeutic approach for oral cancer through JNK1/2- and p38-mediated caspase activation. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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13 pages, 5014 KiB

Open AccessArticle

Ailanthoidol, a Neolignan, Suppresses TGF-β1-Induced HepG2 Hepatoblastoma Cell Progression

by Tsui-Hwa Tseng, Huei-Jane Lee, Yean-Jang Lee, Ko-Chao Lee, Chien-Heng Shen and Hsing-Chun Kuo

Biomedicines 2021, 9(9), 1110; https://doi.org/10.3390/biomedicines9091110 - 30 Aug 2021

Cited by 6 | Viewed by 2228

Abstract

Ailanthoidol (ATD), a neolignan, possessed an antitumor promotion effect in the mouse skin model in our previous investigation. However, other antitumor properties remain to be elucidated. Liver cancer is a major cause of death in the world, and its prognosis and survival rate are poor. Therefore, the prevention and therapy of liver cancer have received much attention. TGF (transforming growth factor)-β1, a cytokine, plays a critical role in the progression of liver cancer. This study determined the inhibitory effects of ATD on the migration and invasion induced by TGF-β1 in HepG2 hepatoblastoma cells. Furthermore, ATD reduced the TGF-β1-promoted colony number of HepG2 hepatoblastoma cells. In addition to reversing TGF-β1-induced cell scattering, ATD suppressed TGF-β1-induced expression of integrin α3, vimentin, N-cadherin, and matrix metalloproteinase 2 (MMP2). Finally, this study found that ATD significantly inhibited TGF-β1-promoted phosphorylation of p-38 mitogen-activated protein kinase (MAPK) and Smad 2. Furthermore, the administration of SB203580 (p38MAPK inhibitor) suppressed TGF-β1-induced expression of integrin α3, N-cadherin, and MMP2. These results demonstrate a novel mechanism of ATD against progression of liver cancer. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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Review

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13 pages, 1195 KiB

Open AccessReview

CXCR1: A Cancer Stem Cell Marker and Therapeutic Target in Solid Tumors

by Caitlin Molczyk and Rakesh K. Singh

Biomedicines 2023, 11(2), 576; https://doi.org/10.3390/biomedicines11020576 - 16 Feb 2023

Cited by 4 | Viewed by 2064

Abstract

Therapy resistance is a significant concern while treating malignant disease. Accumulating evidence suggests that a subset of cancer cells potentiates tumor survival, therapy resistance, and relapse. Several different pathways regulate these purported cancer stem cells (CSCs). Evidence shows that the inflammatory tumor microenvironment plays a crucial role in maintaining the cancer stem cell pool. Typically, in the case of the tumor microenvironment, inflammatory pathways can be utilized by the tumor to aid in tumor progression; one such pathway is the CXCR1/2 pathway. The CXCR1 and CXCR2 receptors are intricately related, with CXCR1 binding two ligands that also bind CXCR2. They have the same downstream pathways but potentially separate roles in the tumor microenvironment. CXCR1 is becoming more well known for its role as a cancer stem cell identifier and therapeutic target. This review elucidates the role of the CXCR1 axis as a CSC marker in several solid tumors and discusses the utility of CXCR1 as a therapeutic target. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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23 pages, 1634 KiB

Open AccessReview

Targeting the Tumor Microenvironment in Acute Myeloid Leukemia: The Future of Immunotherapy and Natural Products

by Christopher Hino, Bryan Pham, Daniel Park, Chieh Yang, Michael H.K. Nguyen, Simmer Kaur, Mark E. Reeves, Yi Xu, Kevin Nishino, Lu Pu, Sue Min Kwon, Jiang F. Zhong, Ke K. Zhang, Linglin Xie, Esther G. Chong, Chien-Shing Chen, Vinh Nguyen, Dan Ran Castillo and Huynh Cao

Biomedicines 2022, 10(6), 1410; https://doi.org/10.3390/biomedicines10061410 - 14 Jun 2022

Cited by 4 | Viewed by 3701

Abstract

The tumor microenvironment (TME) plays an essential role in the development, proliferation, and survival of leukemic blasts in acute myeloid leukemia (AML). Within the bone marrow and peripheral blood, various phenotypically and functionally altered cells in the TME provide critical signals to suppress the anti-tumor immune response, allowing tumor cells to evade elimination. Thus, unraveling the complex interplay between AML and its microenvironment may have important clinical implications and are essential to directing the development of novel targeted therapies. This review summarizes recent advancements in our understanding of the AML TME and its ramifications on current immunotherapeutic strategies. We further review the role of natural products in modulating the TME to enhance response to immunotherapy. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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20 pages, 1472 KiB

Open AccessReview

Natural Compounds Targeting Cancer-Associated Fibroblasts against Digestive System Tumor Progression: Therapeutic Insights

by Kuan-Jung Chiu, Hsin-Ying Clair Chiou, Chi-Han Huang, Pin-Chun Lu, Hui-Ru Kuo, Jiunn-Wei Wang and Ming-Hong Lin

Biomedicines 2022, 10(3), 713; https://doi.org/10.3390/biomedicines10030713 - 19 Mar 2022

Cited by 14 | Viewed by 3248

Abstract

Cancer-associated fibroblasts (CAFs) are critical for cancer occurrence and progression in the tumor microenvironment (TME), due to their versatile roles in extracellular matrix remodeling, tumor–stroma crosstalk, immunomodulation, and angiogenesis. CAFs are the most abundant stromal component in the TME and undergo epigenetic modification and abnormal signaling cascade activation, such as transforming growth factor-β (TGF-β) and Wnt pathways that maintain the distinct phenotype of CAFs, which differs from normal fibroblasts. CAFs have been considered therapeutic targets due to their putative oncogenic functions. Current digestive system cancer treatment strategies often result in lower survival outcomes and fail to prevent cancer progression; therefore, comprehensive characterization of the tumor-promoting and -restraining CAF activities might facilitate the design of new therapeutic approaches. In this review, we summarize the enormous literature on natural compounds that mediate the crosstalk of CAFs with digestive system cancer cells, discuss how the biology and the multifaceted functions of CAFs contribute to cancer progression, and finally, pave the way for CAF-related antitumor therapies. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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18 pages, 3548 KiB

Open AccessReview

Anticancer Targets and Signaling Pathways Activated by Britannin and Related Pseudoguaianolide Sesquiterpene Lactones

by Christian Bailly

Biomedicines 2021, 9(10), 1325; https://doi.org/10.3390/biomedicines9101325 - 26 Sep 2021

Cited by 10 | Viewed by 2834

Abstract

Sesquiterpene lactones (SLs) are abundant in plants and display a large spectrum of bioactivities. The compound britannin (BRT), found in different Inula species, is a pseudoguaianolide-type SL equipped with a typical and highly reactive α-methylene-γ-lactone moiety. The bioproperties of BRT and related pseudoguaianolide SLs, including helenalin, gaillardin, bigelovin and others, have been reviewed. Marked anticancer activities of BRT have been evidenced in vitro and in vivo with different tumor models. Three main mechanisms are implicated: (i) interference with the NFκB/ROS pathway, a mechanism common to many other SL monomers and dimers; (ii) blockade of the Keap1-Nrf2 pathway, with a covalent binding to a cysteine residue of Keap1 via the reactive α-methylene unit of BRT; (iii) a modulation of the c-Myc/HIF-1α signaling axis leading to a downregulation of the PD-1/PD-L1 immune checkpoint and activation of cytotoxic T lymphocytes. The non-specific reactivity of the α-methylene-γ-lactone moiety with the sulfhydryl groups of proteins is discussed. Options to reduce or abolish this reactivity have been proposed. Emphasis is placed on the capacity of BRT to modulate the tumor microenvironment and the immune-modulatory action of the natural product. The present review recapitulates the anticancer effects of BRT, some central concerns with SLs and discusses the implication of the PD1/PD-L1 checkpoint in its antitumor action. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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Other

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16 pages, 1802 KiB

Open AccessEditor’s ChoiceSystematic Review

Combination of Conventional Drugs with Biocompounds Derived from Cinnamic Acid: A Promising Option for Breast Cancer Therapy

by Lyvia Eloiza de Freitas Meirelles, Maria Vitória Felipe de Souza, Lucimara Rodrigues Carobeli, Fabrício Morelli, Natália Lourenço Mari, Edilson Damke, Cristiane Suemi Shinobu Mesquita, Jorge Juarez Vieira Teixeira, Marcia Edilaine Lopes Consolaro and Vânia Ramos Sela da Silva

Biomedicines 2023, 11(2), 275; https://doi.org/10.3390/biomedicines11020275 - 19 Jan 2023

Cited by 5 | Viewed by 2124

Abstract

Despite the options available for breast cancer (BC) therapy, several adverse effects and resistance limit the success of the treatment. Furthermore, the use of a single drug is associated with a high failure rate. We investigated through a systematic review the in vitro effects of the combination between conventional drugs and bioactive compounds derived from cinnamic acid in BC treatment. The information was acquired from the following databases: PubMed, Web of Science, Embase, Scopus, Lilacs and Cochrane library. We focused on “Cinnamates”, “Drug Combinations” and “Breast neoplasms” for publications dating between January 2012 and December 2022, based on the PRISMA statement. The references of the articles were carefully reviewed. Finally, nine eligible studies were included. The majority of these studies were performed using MCF-7, MDA-MB-231, MDA-MB-468 and BT-20 cell lines and the combination between cisplatin, paclitaxel, doxorubicin, tamoxifen, dactolisib and veliparib, with caffeic acid phenethyl ester, eugenol, 3-caffeoylquinic acid, salvianolic acid A, ferulic acid, caffeic acid, rosmarinic acid and ursolic acid. The combination improved overall conventional drug effects, with increased cytotoxicity, antimigratory effect and reversing resistance. Combining conventional drugs with bioactive compounds derived from cinnamic acid could emerge as a privileged scaffold for establishing new treatment options for different BC types. Full article

(This article belongs to the Special Issue Tumor Microenvironment Regulation and Anti-cancer Natural Products)

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