Cancer Cell Communications, Metastasis, and Survival in Host Microenvironment

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 3010

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Guest Editor
Graduate Institute of Biomedical Sciences, College of Medicine, China Medical University, Taichung 40402, Taiwan
Interests: Alzheimer’s disease; WWOX; tumor suppressor; peptide drugs; cancer; cancer-induced neurodegeneration
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Special Issue Information

Dear Colleagues,

Cancer metastasis is responsible for approximately 90% cancer death1. When an invading cancer cell migrates out of the primary solid tumor, this cell faces unfriendly host cells in the microenvironment2,3. WW domain-containing oxidoreductase (WWOX)-deficient or-dysfunctional cancer cells, designated WWOXd2,3, are mainly metastatic, and cannot recognize host cells and parental cancer cells. These metastatic cancer cells are able to dodge, compromise, and cause damage to the WWOX-functional normal host cells or parental cancer cells (WWOXf) from a distance2,3. WWOXf cells are either normal cells or benign cancer cells2,3.

WWOXf cells migrate collectively and expel the individually migrating WWOXd cells. WWOXd cells, in turn, kill a portion of WWOXf cells from a distance by significantly upregulating redox activity in WWOXf cells for leading to cell death2,3. It is reasonable to assume that metastatic WWOXd cells are repelled, in part, by the parental WWOXf cells in the primary tumor, and then leave the home base. From a remote distance, WWOXf cells induce WWOXd cells to activate MIF, Hyal-2, Eph, and Wnt signaling pathways, followed by converging to the MEK/ERK signaling that enables WWOXd cells to undergo retrograde migration to evade WWOXf cells2,3. Exogenous TGF-β assists WWOXd cells to migrate forward in a collective manner and then merge with WWOXf cells, suggesting that TGF-β derived from metastatic WWOXd cells enhances the recognition and merging between WWOXd and WWOXf cell2,3.

In this call for research and review papers 2023, the specific topic will focus on gene alterations that contribute to changes in cancer cell migratory behavior, cell-to-cell recognition and communication, cancer cell-host cell functional antagonism, and cell survival in host microenvironment. We welcome articles related, but not limited, to

(1) gene alteration-induced cancer cell metastasis and the underlined signaling pathways;

(2) metastatic cancer cell and host cell recognition;

(3) metastatic cancer cell modification of host microenvironment;

(4) cancer cell-derived cytokines and/or exosomes in attacking host cells;

(5) molecular mechanisms by which host cells fight back to kill metastatic cancer cells;

(6) whether and how metastatic cancer cells and host cells compromise each other so that metastatic cancer cells can build a new home base in a target organ;

(7) innovative methodologies to measure metastatic cancer cell and host cell recognition and communication.  

  1. Fares, J.; Fares, M.Y.; Khachfe, H.H.; Salhab, H.A.; Fares, Y. Molecular principles of metastasis: A hallmark of cancer revisited. Signal Transduct. Target Ther. 2020, 5, 28.
  2. Chen, Y.A.; Sie, Y.D.; Liu, T.Y.; Kuo, H.L.; Chou, P.Y.; Chen, Y.J.; Lee, K.T.; Chen, P.J.; Chen, S.T.; Chang, N.S. Normal cells repel WWOX-negative or -dysfunctional cancer cells via WWOX cell surface epitope 286-299. Commun. Biol. 2021, 4, 1–19.
  3. Chou, P.Y.; Lai, F.J.; Chen, Y.A.; Sie, Y.D.; Kuo, H.L.; Su, W.P.; Wu, C.Y.; Liu, T.Y.; Wen, K.Y.; Hsu, L.J.; et al. Strategies by which WWOX-deficient metastatic cancer cells utilize to survive via dodging, compromising, and causing damage to WWOX-positive normal microenvironment. Cell Death Discov. 2019, 5, 97.

Dr. Nan-Shan Chang
Guest Editor

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Published Papers (2 papers)

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Research

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29 pages, 6918 KiB  
Article
Controlled Plasma Membrane Delivery of FGFR1 and Modulation of Signaling by a Novel Regulated Anterograde RTK Transport Pathway
by Claire Leist Hinsch, Jagadish Kummetha Venkata, Tien Hsu and Vincent Dammai
Cancers 2023, 15(24), 5837; https://doi.org/10.3390/cancers15245837 - 14 Dec 2023
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Abstract
How human FGFR1 localizes to the PM is unknown. Currently, it is assumed that newly synthesized FGFR1 is continuously delivered to the PM. However, evidence indicates that FGFR1 is mostly sequestered in intracellular post-Golgi vesicles (PGVs) under normal conditions. In this report, live-cell [...] Read more.
How human FGFR1 localizes to the PM is unknown. Currently, it is assumed that newly synthesized FGFR1 is continuously delivered to the PM. However, evidence indicates that FGFR1 is mostly sequestered in intracellular post-Golgi vesicles (PGVs) under normal conditions. In this report, live-cell imaging and total internal reflection fluorescence microscopy (TIRFM) were employed to study the dynamics of these FGFR1-positive vesicles. We designed recombinant proteins to target different transport components to and from the FGFR1 vesicles. Mouse embryoid bodies (mEBs) were used as a 3D model system to confirm major findings. Briefly, we found that Rab2a, Rab6a, Rab8a, RalA and caveolins are integral components of FGFR1-positive vesicles, representing a novel compartment. While intracellular sequestration prevented FGFR1 activation, serum starvation and hypoxia stimulated PM localization of FGFR1. Under these conditions, FGFR1 C-terminus acts as a scaffold to assemble proteins to (i) inactivate Rab2a and release sequestration, and (ii) assemble Rab6a for localized activation of Rab8a and RalA-exocyst to deliver the receptor to the PM. This novel pathway is named Regulated Anterograde RTK Transport (RART). This is the first instance of RTK regulated through control of PM delivery. Full article
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11 pages, 978 KiB  
Review
A Review of Herbal Resources Inducing Anti-Liver Metastasis Effects in Gastrointestinal Tumors via Modulation of Tumor Microenvironments in Animal Models
by Sul-Ki Kim, Nam-Hun Lee and Chang-Gue Son
Cancers 2023, 15(13), 3415; https://doi.org/10.3390/cancers15133415 - 29 Jun 2023
Cited by 1 | Viewed by 1471
Abstract
Liver metastases remain a major obstacle for the management of all types of tumors arising from digestive organs, and the tumor microenvironment has been regarded as an important factor in metastasis. To discover herbal candidates inhibiting the liver metastasis of tumors originating from [...] Read more.
Liver metastases remain a major obstacle for the management of all types of tumors arising from digestive organs, and the tumor microenvironment has been regarded as an important factor in metastasis. To discover herbal candidates inhibiting the liver metastasis of tumors originating from the digestive system via the modulation of the tumor microenvironment and liver environment, we searched three representative public databases and conducted a systematic review. A total of 21 studies that employed experimental models for pancreatic (9), colon (8), and stomach cancers (4) were selected. The herbal agents included single-herb extracts (5), single compounds (12), and multiherbal decoctions (4). Curcuma longa Linn was most frequently studied for its anti-colon–liver metastatic effects, and its possible mechanisms involved the modulation of tumor microenvironment components such as vascular endothelial cells and immunity in both tumor tissues and circulating cells. The list of herbal agents and their mechanisms produced in this study is helpful for the development of anti-liver metastasis drugs in the future. Full article
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