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Cytokines/Chemokines in Cancer Metastasis 2.0
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Cytokines/Chemokines in Cancer Metastasis 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 (31 May 2022) | Viewed by 28967

Special Issue Editor

Dr. Mohd W. Nasser

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198-5870, USA
Interests: chemokines; cytokines; microRNAs; noncoding RNAs; breast cancer; lung cancer; brain metastasis; metastasis; experimental therapeutics; nanotechnology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The survival of the majority of patients with solid tumors has increased due to advances in diagnosis, imaging, surgery, and therapy. However, cancer metastasis is the leading cause of cancer-related deaths. There is an urgent need to understand the biology of metastasis for the development of novel preventive/therapeutic approaches for controlling metastasis to distant organs. Cancer cells release cytokines or chemokines that will communicate through their receptors present on stromal (paracrine mechanism) and cancer cells (autocrine mechanism). An altered expression profile of chemokines/cytokines regulates angiogenesis, proliferation, and metastasis at various stages in the solid tumors. It has been shown that blocking chemokines/cytokines or their cognate receptors plays a significant role in controlling cancer progression/metastasis. In addition, cytokines and chemokines can be used to improve the response of chimeric antigen receptor (CAR)-T cells against solid malignancies. The papers in the current Special Issue will cover all the topics of chemokines/cytokines and their role in the tumor microenvironment and blocking strategies of these axes as a monotherapy and combination therapies for the prevention of metastasis.

Dr. Mohd W. Nasser
Guest Editor

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Keywords

  • Chemokines
  • Chemokine receptors
  • Cytokines
  • Cytokine receptors
  • CAR-T cell therapy
  • Immunotherapy
  • Cytokine therapy
  • Chemokine therapy
  • Angiogenesis
  • Vascular co-option
  • Interleukins
  • Tumor-associated macrophages
  • Myeloid-derived suppressor cells
  • NK-cells
  • Regulatory T-cells (Treg)
  • Cytotoxic T-cells

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Published Papers (5 papers)

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Research

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15 pages, 3298 KiB  
Article
Azithromycin and Ceftriaxone Differentially Activate NLRP3 in LPS Primed Cancer Cells
by Gulcin Tezcan, Mohammad Alsaadi, Shaimaa Hamza, Ekaterina E. Garanina, Ekaterina V. Martynova, Gulshat R. Ziganshina, Elina R. Farukshina, Albert A. Rizvanov and Svetlana F. Khaiboullina
Int. J. Mol. Sci. 2022, 23(16), 9484; https://doi.org/10.3390/ijms23169484 - 22 Aug 2022
Cited by 1 | Viewed by 3313
Abstract
Background: Cancer patients are prescribed antibiotics, such as macrolides and lactamides, for infection treatment. However, the effect of these antibiotics on NLRP3 activation remains largely unknown. Method: Lung cancer (A549) and prostate cancer (PC3) cell lines were primed with lipopolysaccharide (LPS) to activate [...] Read more.
Background: Cancer patients are prescribed antibiotics, such as macrolides and lactamides, for infection treatment. However, the effect of these antibiotics on NLRP3 activation remains largely unknown. Method: Lung cancer (A549) and prostate cancer (PC3) cell lines were primed with lipopolysaccharide (LPS) to activate NLRP3 transcription. Cells were then treated with azithromycin (Az) or ceftriaxone (Cf). NLRP3 activation was analyzed by qPCR, Western blot, and ELISA. Cell growth and viability were assessed by real-time cell analysis and Annexin V expression. Levels of 41 cytokines were also analyzed using a multiplex assay. Results: LPS-Az activated transcription of NLRP3, Pro-CASP-1, and Pro-IL-1β in A549 cells, while failing to upregulate NLRP3 and Pro-IL-1β in PC3 cells. LPS-Az decreased the secretion of pro-inflammatory cytokines while it induced the pro-angiogenic factors in A549 and PC3 cells. In contrast, LPS-Cf suppressed the expression of NLRP3-associated genes, NLRP3 protein expression, the inflammatory cytokine secretion in A549 and PC3 cells. LPS-Az and LPS-Cf had a limited effect on cell growth and viability. Discussion: Our data suggest that Cf could suppress LPS induced NLRP3, which should be considered when selecting antibiotics for cancer treatment. In contrast, the effect of Az on LPS primed NLRP3 and the inflammatory cytokines production appears to depend on the cancer cell origin. Therefore, these data indicate that considerations are required when selecting Az for the treatment of cancer patients. Full article
(This article belongs to the Special Issue Cytokines/Chemokines in Cancer Metastasis 2.0)
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14 pages, 10456 KiB  
Article
Discoidin Domain Receptor 2 Mediates Lysophosphatidic Acid-Induced Ovarian Cancer Aggressiveness
by Bo Young Jeong, Kyung Hwa Cho, Se-Hee Yoon, Chang Gyo Park, Hwan-Woo Park and Hoi Young Lee
Int. J. Mol. Sci. 2021, 22(10), 5374; https://doi.org/10.3390/ijms22105374 - 20 May 2021
Cited by 7 | Viewed by 2778
Abstract
Lysophosphatidic acid (LPA), a bioactive lipid produced extracellularly by autotaxin (ATX), has been known to induce various pathophysiological events, including cancer cell invasion and metastasis. Discoidin domain receptor 2 (DDR2) expression is upregulated in ovarian cancer tissues, and is closely associated with poor [...] Read more.
Lysophosphatidic acid (LPA), a bioactive lipid produced extracellularly by autotaxin (ATX), has been known to induce various pathophysiological events, including cancer cell invasion and metastasis. Discoidin domain receptor 2 (DDR2) expression is upregulated in ovarian cancer tissues, and is closely associated with poor clinical outcomes in ovarian cancer patients. In the present study, we determined a critical role and signaling cascade for the expression of DDR2 in LPA-induced ovarian cancer cell invasion. We also found ectopic expression of ATX or stimulation of ovarian cancer cells with LPA-induced DDR2 expression. However, the silencing of DDR2 expression significantly inhibited ATX- and LPA-induced ovarian cancer cell invasion. In addition, treatment of the cells with pharmacological inhibitors of phosphoinositide 3-kinase (PI3K), Akt, and mTOR abrogated LPA-induced DDR2 expression. Moreover, we observed that HIF-1α, located downstream of the mTOR, is implicated in LPA-induced DDR2 expression and ovarian cancer cell invasion. Finally, we provide evidence that LPA-induced HIF-1α expression mediates Twist1 expression to upregulate DDR2 expression. Collectively, the present study demonstrates that ATX, and thereby LPA, induces DDR2 expression through the activation of the PI3K/Akt/mTOR/HIF-1α/Twist1 signaling axes, aggravating ovarian cancer cell invasion. Full article
(This article belongs to the Special Issue Cytokines/Chemokines in Cancer Metastasis 2.0)
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Review

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16 pages, 319 KiB  
Review
CXCL12-CXCR4/CXCR7 Axis in Colorectal Cancer: Therapeutic Target in Preclinical and Clinical Studies
by Tripti Khare, Marc Bissonnette and Sharad Khare
Int. J. Mol. Sci. 2021, 22(14), 7371; https://doi.org/10.3390/ijms22147371 - 9 Jul 2021
Cited by 72 | Viewed by 6364
Abstract
Chemokines are chemotactic cytokines that promote cancer growth, metastasis, and regulate resistance to chemotherapy. Stromal cell-derived factor 1 (SDF1) also known as C-X-C motif chemokine 12 (CXCL12), a prognostic factor, is an extracellular homeostatic chemokine that is the natural ligand for chemokine receptors [...] Read more.
Chemokines are chemotactic cytokines that promote cancer growth, metastasis, and regulate resistance to chemotherapy. Stromal cell-derived factor 1 (SDF1) also known as C-X-C motif chemokine 12 (CXCL12), a prognostic factor, is an extracellular homeostatic chemokine that is the natural ligand for chemokine receptors C-X-C chemokine receptor type 4 (CXCR4), also known as fusin or cluster of differentiation 184 (CD184) and chemokine receptor type 7 (CXCR7). CXCR4 is the most widely expressed rhodopsin-like G protein coupled chemokine receptor (GPCR). The CXCL12–CXCR4 axis is involved in tumor growth, invasion, angiogenesis, and metastasis in colorectal cancer (CRC). CXCR7, recently termed as atypical chemokine receptor 3 (ACKR3), is amongst the G protein coupled cell surface receptor family that is also commonly expressed in a large variety of cancer cells. CXCR7, like CXCR4, regulates immunity, angiogenesis, stem cell trafficking, cell growth and organ-specific metastases. CXCR4 and CXCR7 are expressed individually or together, depending on the tumor type. When expressed together, CXCR4 and CXCR7 can form homo- or hetero-dimers. Homo- and hetero-dimerization of CXCL12 and its receptors CXCR4 and CXCR7 alter their signaling activity. Only few drugs have been approved for clinical use targeting CXCL12-CXCR4/CXCR7 axis. Several CXCR4 inhibitors are in clinical trials for solid tumor treatment with limited success whereas CXCR7-specific inhibitors are still in preclinical studies for CRC. This review focuses on current knowledge of chemokine CXCL12 and its receptors CXCR4 and CXCR7, with emphasis on targeting the CXCL12–CXCR4/CXCR7 axis as a treatment strategy for CRC. Full article
(This article belongs to the Special Issue Cytokines/Chemokines in Cancer Metastasis 2.0)
18 pages, 2751 KiB  
Review
Cytokines-Biogenesis and Their Role in Human Breast Milk and Determination
by Anna Kiełbasa, Renata Gadzała-Kopciuch and Bogusław Buszewski
Int. J. Mol. Sci. 2021, 22(12), 6238; https://doi.org/10.3390/ijms22126238 - 9 Jun 2021
Cited by 20 | Viewed by 3671
Abstract
Cytokines play a huge role in many biological processes. Their production, release and interactions are subject to a very complex mechanism. Cytokines are produced by all types of cells, they function very differently and they are characterized by synergism in action, antagonism, and [...] Read more.
Cytokines play a huge role in many biological processes. Their production, release and interactions are subject to a very complex mechanism. Cytokines are produced by all types of cells, they function very differently and they are characterized by synergism in action, antagonism, and aggregation activity, opposing action of one cytokine, overlapping activity, induction of another cytokine, inhibition of cytokine synthesis at the mRNA level as well as autoregulation-stimulation or inhibition of own production. The predominance of pro-inflammatory cytokines leads to a systemic inflammatory response, and anti-inflammatory-to an anti-inflammatory response. They regulate the organism’s immune response and protect it against sudden disturbances in homeostasis. The synthesis and activity of cytokines are influenced by the central nervous system through the endocrine system (pituitary gland, adrenal glands). Full article
(This article belongs to the Special Issue Cytokines/Chemokines in Cancer Metastasis 2.0)
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19 pages, 2234 KiB  
Review
Clinical Implications of Exosomes: Targeted Drug Delivery for Cancer Treatment
by Andrew E. Massey, Shabnam Malik, Mohammad Sikander, Kyle A. Doxtater, Manish K. Tripathi, Sheema Khan, Murali M. Yallapu, Meena Jaggi, Subhash C. Chauhan and Bilal B. Hafeez
Int. J. Mol. Sci. 2021, 22(10), 5278; https://doi.org/10.3390/ijms22105278 - 17 May 2021
Cited by 20 | Viewed by 11919
Abstract
Exosomes are nanoscale vesicles generated by cells for intercellular communication. Due to their composition, significant research has been conducted to transform these particles into specific delivery systems for various disease states. In this review, we discuss the common isolation and loading methods of [...] Read more.
Exosomes are nanoscale vesicles generated by cells for intercellular communication. Due to their composition, significant research has been conducted to transform these particles into specific delivery systems for various disease states. In this review, we discuss the common isolation and loading methods of exosomes, some of the major roles of exosomes in the tumor microenvironment, as well as discuss recent applications of exosomes as drug delivery vessels and the resulting clinical implications. Full article
(This article belongs to the Special Issue Cytokines/Chemokines in Cancer Metastasis 2.0)
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