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Infection, Inflammation and Cancer

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A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 32263

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Dr. Imran Khan

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The Hormel Institute, University of Minnesota, Austin, MN 55912, USA
Interests: cancer cells; tumor microenvironment; cancer biology; cell culture; tumor biology; tumor cell culture, anti-microbial, anti-inflammation, host-microbe interaction
Special Issues, Collections and Topics in MDPI journals

Dr. Faisal Aziz

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Guest Editor

The Hormel Institute, University of Minnesota, Austin, MN 55912, USA
Interests: inflammation and cancer biology; immunology and bacterial pathogenesis; mitochondrial metabolism; post-translational modification; dietary agents; drug discovery; protein structure biology; life-style and environmental cancer; risk factors
Special Issues, Collections and Topics in MDPI journals

Dr. Anil K Yadav

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Dr. Ajay S. Akhade

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Guest Editor

Institute for Systems Biology, University of Washington, Seattle, WA 98109, USA
Interests: microbial pathogenesis; innate immunity; inflammation; host-pathogen interaction; autoinflammatory disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Nobel prize winner Johannes Fibiger, in 1926, discovered that stomach cancer in rats was caused by nematode parasites, indicating the very first link between cancer and infectious agents. The link has grown stronger with the additional Nobel-winning discoveries of Helicobacter pylori (gastric cancer) and papillomavirus (cervical cancer). It is projected that one in five cases of cancer is triggered by an infection or inflammation. It is crucial to reveal the role of infection and inflammation, as well as the underlying mechanism(s) responsible for cancer progression. Therefore, this Special Issue focuses on our current understanding of the infection or inflammation signaling cascade, its link to cancer progression, and the therapeutic approaches currently available. We invite researchers to contribute research articles or reviews dealing with molecular/cellular biology, immunology, and the epidemiology of the link between infection/inflammation and cancer.

Potential topics include:

Basic research on the molecular mechanisms of infection or inflammation or cancer.
Development of novel drug treatment approaches for infection- or inflammation-related cancer triggers.
Formulation of advanced, nanomedicine, or combination treatment approaches for infection- and/or inflammation-related cancers.
Identification of novel pathogens in infection- and/or inflammation-induced cancer.
Inflammatory signaling pathways such as MAPK, NF-κB, JAK-STAT, PI3K-AKT, etc.

We look forward to your contributions to this Special Issue, which will encourage further developments in this exhilarating field.

Dr. Imran Khan
Dr. Faisal Aziz
Dr. Anil K Yadav
Dr. Ajay Suresh Akhade
Guest Editors

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Keywords

molecular/cellular biology
immunology
infection
cancer

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Published Papers (11 papers)

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Research

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20 pages, 2857 KiB

Open AccessArticle

Gold Nanoparticles Inhibit PMA-Induced MMP-9 Expression via microRNA-204-5p Upregulation and Deactivation of NF-κBp65 in Breast Cancer Cells

by Aisha Farhana, Abdullah Alsrhani, Nazia Nazam, Muhammad Ikram Ullah, Yusuf Saleem Khan and Zafar Rasheed

Biology 2023, 12(6), 777; https://doi.org/10.3390/biology12060777 - 27 May 2023

Cited by 7 | Viewed by 2026

Abstract

Objective: Breast cancer (BC) is the most common malignancy in females globally. Matrix metalloproteinase-9 (MMP-9) is crucial to the invasion, progression and spread of BC. Gold nanoparticles (AuNPs) have an anti-tumorigenic role, but their therapeutic role in microRNAs (miRNAs) regulation has not been explored. This study determined the potential of AuNPs against MMP-9 overexpression/production and miRNA-204-5p regulation in BC cells. Methods: AuNPs were newly engineered, and their stability was analyzed using the zeta potential, polydispersity index, surface-plasmon-resonance peak and transmission electron microscopy. A bioinformatics algorithm was used to predict the pairing of miRNA in the 3′untranslated-region (3′UTR) of MMP-9 mRNA. TaqMan assays were carried out to quantify miRNA and mRNA, whereas MMP-9-specific immunoassays and gelatin zymography were used to determine protein secretion and activity. The binding of miRNA in MMP-9 mRNA 3′UTR was verified by luciferase reporter clone assays and transfection with anti-miRNAs. In addition, NF-κBp65 activity was determined and confirmed with parthenolide treatment. Results: Engineered AuNPs were highly stable and spherical in shape, with a mean size of 28.3 nm. Tested in MCF-7 BC cells, microRNA-204-5p directly regulates MMP-9. AuNPs inhibit PMA-induced MMP-9 mRNA and protein via hsa-miR-204-5p upregulation. Anti-miR-204 transfected MCF-7 cells demonstrated enhanced MMP-9 expression (p < 0.001), while AuNPs treatment attenuated MMP-9 expression in a dose-dependent manner (p < 0.05). Moreover, AuNPs also inhibit PMA-induced NF-κBp65 activation in anti-hsa-miR-204 transfected MCF-7 cells. Conclusion: Engineered AuNPs were stable and non-toxic to BC cells. AuNPs inhibit PMA-induced MMP-9 expression, production and activation via NF-κBp65 deactivation and hsa-miR-204-5p upregulation. These novel therapeutic potentials of AuNPs on stimulated BC cells provide novel suggestions that AuNPs inhibit carcinogenic activity via inverse regulation of microRNAs. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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15 pages, 4016 KiB

Open AccessArticle

Effects of Intermediate Frequency (150 kHz) Electromagnetic Radiation on the Vital Organs of Female Sprague Dawley Rats

by Venkatesan Sundaram, Stephanie Mohammed, Brian N. Cockburn, M. R. Srinivasan, Chalapathi R. Adidam Venkata, Jenelle Johnson, Lester Gilkes, Kegan Romelle Jones and Nikolay Zyuzikov

Biology 2023, 12(2), 310; https://doi.org/10.3390/biology12020310 - 14 Feb 2023

Cited by 4 | Viewed by 2379 | Correction

Abstract

Exposure to electromagnetic radiation (EMR) from intermediate frequency sources has increased exponentially in recent years. The consequences of this exposure on biological systems are prompting scientists to study the effects on human health. This current study aimed to determine the effects of intermediate frequency (150 kHz) EMR exposure on the vital organs of female Sprague Dawley rats. The EMR group (n = 10 animals) was exposed to a frequency of 150 kHz with an intensity of 65 ± 15 μW/cm² for two months. The control group (n = 10 animals) was exposed to an intensity of 35 ± 15 nW/cm². Haematological, histochemical, gross, and histopathological profiles of all major organs of all animals were then performed using standard procedures. All major organs generally showed no significant detectable effects in either the control or EMR groups. However, gross and histopathological examinations revealed the effects of EMR on the liver and lungs, which showed inflammatory changes without significant biochemical/haematological manifestations. In addition, a significant increase in serum sodium level and a decrease in serum urea level were also observed in the EMR group. It can be concluded that the current frequency and duration of exposure trigger the changes in the liver and lungs but are not sufficient to cause clinical and functional manifestations. Therefore, a long-term exposure study might be helpful to determine the effects of 150 kHz IF EMR on these organs. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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20 pages, 3136 KiB

Open AccessArticle

Transcriptomic Analysis of Hepatitis B Infected Liver for Prediction of Hepatocellular Carcinoma

by Diren Arda Karaoglu, Meral Uner, Cem Simsek, Ali Osmay Gure and Secil Demirkol-Canli

Biology 2023, 12(2), 188; https://doi.org/10.3390/biology12020188 - 26 Jan 2023

Cited by 1 | Viewed by 2770

Abstract

Hepatocellular cancer (HCC) is a leading cause of cancer-related mortality worldwide, and chronic hepatitis B virus infection (CHB) has been a major risk factor for HCC development. The pathogenesis of HBV-related HCC has been a major focus revealing the interplay of a multitude of intracellular signaling pathways, yet the precise mechanisms and their implementations to clinical practice remain to be elucidated. This study utilizes publicly available transcriptomic data from the livers of CHB patients in order to identify a population with a higher risk of malignant transformation. We report the identification of a novel list of genes (PCM1) which can generate clear transcriptomic sub-groups among HBV-infected livers. PCM1 includes genes related to cell cycle activity and liver cancer development. In addition, markers of inflammation, M1 macrophages and gamma delta T cell infiltration are present within the signature. Genes within PCM1 are also able to differentiate HCC from normal liver, and some genes within the signature are associated with poor prognosis of HCC at the mRNA level. The analysis of the immunohistochemical stainings validated that proteins coded by a group of PCM1 genes were overexpressed in liver cancer, while minimal or no expression was detected in normal liver. Altogether, our findings suggest that PCM1 can be developed into a clinically applicable method to identify CHB patients with a higher risk of HCC development. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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15 pages, 3298 KiB

Open AccessArticle

Chick Early Amniotic Fluid (ceAF) Deters Tumorigenesis via Cell Cycle Arrest and Apoptosis

by Mashaal Ahmad, Jia Yu, Sha Cheng, Zara Ahmad Khan, Yan Luo and Heng Luo

Biology 2022, 11(11), 1577; https://doi.org/10.3390/biology11111577 - 27 Oct 2022

Cited by 1 | Viewed by 1960

Abstract

In recent years, amniotic fluids have gained attention in cancer research. They have an influential role in protecting embryos against several anomalies. Chick early amniotic fluid (ceAF)—amniotic fluid isolated from growing chicken—has been used in many other studies, including myocardial infarctions and skin regeneration. In this study, we employed ceAF’s promising therapeutic applications against tumorigenesis in both in vitro and in vivo studies. We selected three robust proliferating tumor cell lines: BCaP37, MCF7, and RKO. We found that selective dosage is required to obtain maximum impact to deter tumorigenesis. ceAF not only disrupted the uniform colonies of tumor cell lines via disturbing mitochondrial transmembrane potential, but also arrested many cells at growing G1 state via working agonistically with aphidicolin. The significant inhibition of tumor metastasis by ceAF was indicated by in vivo models. This leads to apoptosis analysis as verified by annexin-V staining stays and immunoblotting of critical proteins as cell cycle meditators and apoptosis regulators. Not only on the protein level, but we also tested ceAF’s therapeutic potentials on mRNA levels as indicated by quantitative real-time PCR summarizing the promising role of ceAF in deterring tumor progression. In conclusion, our study reveals the potent role of ceAF against tumorigenesis in breast cancer and colon carcinoma. Further studies will be required to determine the critical components present in ceAF and its purification to narrow down this study. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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13 pages, 339 KiB

Open AccessArticle

Assessment of Specific Tumoral Markers, Inflammatory Status, and Vitamin D Metabolism before and after the First Chemotherapy Cycle in Patients with Lung Cancer

by Andreea Crintea, Cristina Drugan, Anne-Marie Constantin, Iulia Lupan, Zsolt Fekete, Ciprian Nicolae Silaghi and Alexandra Mărioara Crăciun

Biology 2022, 11(7), 1033; https://doi.org/10.3390/biology11071033 - 8 Jul 2022

Cited by 2 | Viewed by 2206

Abstract

Background: We aimed to investigate the changes of inflammatory status reflected by serum levels of chitotriosidase (CHT) and neopterin, and how specific tumor markers such as neuron-specific enolase (NSE) and squamous cell carcinoma antigen (SCCA), as well as vitamin D metabolism assessed by vitamin D receptor (VDR) and 25-hydroxy vitamin D₃ (25OHD₃), were modified after the first cycle of chemotherapy in patients with lung cancer. Methods: We performed this first pilot study on twenty patients diagnosed with lung cancer by investigating the serum concentrations of CHT, neopterin, NSE, SCCA, VDR and 25OHD₃ before and after the first cycle of chemotherapy. Results: The post-treatment values of NSE were significantly lower compared to the pre-treatment levels (14.37 vs. 17.10 ng/mL, p = 0.031). We noticed a similar trend in neopterin levels, but the difference was only marginally significant (1.44 vs. 1.17 ng/mL, p = 0.069). On the contrary, the variations of circulating SCCA, CHT, neopterin, VDR and 25OHD₃, before and after treatment, did not reach statistical significance. Conclusion: Only circulating NSE was treatment responsive to the first chemotherapy cycle in patients with lung cancer, while inflammatory markers and vitamin D status were not significantly modified. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

12 pages, 3016 KiB

Open AccessArticle

Expression and Role of β3-Adrenergic Receptor during the Differentiation of 3T3-L1 Preadipocytes into Adipocytes

by Amir Roshanzadeh, Anil Kumar Yadav, Sai-Prasad Pydi, Takefumi Kimura and Byeong-Churl Jang

Biology 2022, 11(5), 772; https://doi.org/10.3390/biology11050772 - 18 May 2022

Cited by 4 | Viewed by 4002

Abstract

β3-adrenergic receptor (β3-AR) is expressed predominantly in mature white and brown/beige adipocytes. Although the lipolytic and thermogenic role of β3-AR in brown/beige adipocytes is well defined, the adipogenic role of β3-AR in white adipocytes remains unclear at present. In this study, we investigated the expression and function of β3-AR in differentiating 3T3-L1 cells, murine white preadipocytes. Of note, the expression of β3-AR at the protein and mRNA levels was highly induced in a time-dependent manner during 3T3-L1 preadipocyte differentiation. Interestingly, the results of the pharmacological inhibition study demonstrated the roles of p38 MAPK and PKC in the induction of β3-AR expression in differentiating 3T3-L1 cells. Knockdown of β3-AR led to less lipid accumulation and triglyceride (TG) content during 3T3-L1 preadipocyte differentiation with no cytotoxicity. Furthermore, knockdown of β3-AR resulted in a decrease in not only expression levels of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), fatty acid synthase (FASN), perilipin A, and leptin but also phosphorylation levels of signal transducer and activator of transcription-5 (STAT-5) during 3T3-L1 preadipocyte differentiation. In summary, these results demonstrate firstly that β3-AR expression is highly up-regulated in p38 MAPK and PKC-dependent manners, and the up-regulated β3-AR plays a crucial role in lipid accumulation in differentiating 3T3-L1 cells, which is mediated through control of expression and phosphorylation levels of C/EBP-α, PPAR-γ, STAT-5, FASN, and perilipin A. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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Review

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12 pages, 917 KiB

Open AccessReview

Tumor Microenvironment—A Short Review of Cellular and Interaction Diversity

by Aleksandra Bożyk, Kamila Wojas-Krawczyk, Paweł Krawczyk and Janusz Milanowski

Biology 2022, 11(6), 929; https://doi.org/10.3390/biology11060929 - 18 Jun 2022

Cited by 49 | Viewed by 4893

Abstract

The tumor microenvironment is a complex network of various interactions between immune cells and non-cellular components such as the extracellular matrix, exosomes and interleukins. Moreover, tumor heterogeneity and its constant modification may alter the immunophenotype and become responsible for its resistance regarding the therapies applied However, it should be remembered that in a strongly immunosuppressive neoplastic microenvironment, the immune system cells undergo reprogramming and most often cease to fulfill their original function. Therefore, understanding what happens within the tumor microenvironment, and which mechanisms are responsible for tumor development and progression should let us know how cancer could protect itself against the immune system. The presented review summarizes the latest information on the interactions between the tumor microenvironment and the cellular and non-cellular components, as well as their impact on cancer development, progression and immune system exhaustion. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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44 pages, 618 KiB

Open AccessReview

Cancer-Associated Microbiota: From Mechanisms of Disease Causation to Microbiota-Centric Anti-Cancer Approaches

by Priyankar Dey and Saumya Ray Chaudhuri

Biology 2022, 11(5), 757; https://doi.org/10.3390/biology11050757 - 16 May 2022

Cited by 20 | Viewed by 4349

Abstract

Helicobacter pylori infection is the only well-established bacterial cause of cancer. However, due to the integral role of tissue-resident commensals in maintaining tissue-specific immunometabolic homeostasis, accumulated evidence suggests that an imbalance of tissue-resident microbiota that are otherwise considered as commensals, can also promote various types of cancers. Therefore, the present review discusses compelling evidence linking tissue-resident microbiota (especially gut bacteria) with cancer initiation and progression. Experimental evidence supporting the cancer-causing role of gut commensal through the modulation of host-specific processes (e.g., bile acid metabolism, hormonal effects) or by direct DNA damage and toxicity has been discussed. The opportunistic role of commensal through pathoadaptive mutation and overcoming colonization resistance is discussed, and how chronic inflammation triggered by microbiota could be an intermediate in cancer-causing infections has been discussed. Finally, we discuss microbiota-centric strategies, including fecal microbiota transplantation, proven to be beneficial in preventing and treating cancers. Collectively, this review provides a comprehensive understanding of the role of tissue-resident microbiota, their cancer-promoting potentials, and how beneficial bacteria can be used against cancers. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

Other

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2 pages, 470 KiB

Open AccessCorrection

Correction: Sundaram et al. Effects of Intermediate Frequency (150 kHz) Electromagnetic Radiation on the Vital Organs of Female Sprague Dawley Rats. Biology 2023, 12, 310

Biology 2024, 13(3), 181; https://doi.org/10.3390/biology13030181 - 12 Mar 2024

Viewed by 989

Abstract

In the original publication [...] Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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9 pages, 552 KiB

Open AccessOpinion

Innate Immune Recognition, Integrated Stress Response, Infection, and Tumorigenesis

by Klara Kubelkova, Vanda Bostik, Lokesh Joshi and Ales Macela

Biology 2023, 12(4), 499; https://doi.org/10.3390/biology12040499 - 25 Mar 2023

Cited by 6 | Viewed by 2300

Abstract

Engagement of PRRs in recognition of PAMPs or DAMPs is one of the processes that initiates cellular stress. These sensors are involved in signaling pathways leading to induction of innate immune processes. Signaling initiated by PRRs is associated with the activation of MyD88-dependent signaling pathways and myddosome formation. MyD88 downstream signaling depends upon the context of signaling initiation, the cell (sub)type and the microenvironment of signal initiation. Recognition of PAMPs or DAMPs through PRRs activates the cellular autonomous defence mechanism, which orchestrates the cell responses to resolve specific insults at the single cell level. In general, stressed endoplasmic reticulum is directly linked with the induction of autophagy and initiation of mitochondrial stress. These processes are regulated by the release of Ca²⁺ from ER stores accepted by mitochondria, which respond through membrane depolarization and the production of reactive oxygen species generating signals leading to inflammasome activation. In parallel, signaling from PRRs initiates the accumulation of misfolded or inappropriately post-translationally modified proteins in the ER and triggers a group of conserved emergency rescue pathways known as unfolded protein response. The cell-autonomous effector mechanisms have evolutionarily ancient roots and were gradually specialized for the defence of specific cell (sub)types. All of these processes are common to the innate immune recognition of microbial pathogens and tumorigenesis as well. PRRs are active in both cases. Downstream are activated signaling pathways initiated by myddosomes, translated by the cellular autonomous defence mechanism, and finalized by inflammasomes. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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22 pages, 512 KiB

Open AccessSystematic Review

The Role of p16/Ki-67 Immunostaining, hTERC Amplification and Fibronectin in Predicting Cervical Cancer Progression: A Systematic Review

by Septimiu Toader Voidăzan, Caterina Dianzani, Mădălina Aurelia Husariu, Bíborka Geréd, Sabin Gligore Turdean, Cosmina Cristina Uzun, Zsolt Kovacs, Florin Francisc Rozsnyai and Nicoleta Neagu

Biology 2022, 11(7), 956; https://doi.org/10.3390/biology11070956 - 23 Jun 2022

Cited by 10 | Viewed by 2850

Abstract

Human papillomaviruses (HPVs) are common sexually transmitted infectious agents responsible for several anogenital and head and neck cancers. Cervical cancer (CC) is the fourth leading cause of death in women with cancer. The progression of a persistent HPV infection to cancer takes 15–20 years and can be preventable through screening. Cervical cytology (Pap smear) is the standard screening test for CC and precancerous lesions. For ASC-US and ASC-H lesions, a combination of Pap smear and HR-HPV analysis is recommended as a triage step before colposcopy. However, these tests cannot predict progression to CC. For this purpose, we summarized current scientific data on the role of p16/Ki-67 immunohistostaining, telomerase and fibronectin in predicting progression to CC. p16 and p16/Ki-67 dual staining (DS) were more specific than HR-HPV DNA testing for the detection of CIN2+/CIN3+ in women with ASC-US and LSIL. Similarly, hTERC FISH analysis significantly improved the specificity and positive predictive value of HPV DNA testing in differentiating CIN2+ from CIN2 cytological samples. In conclusion, p16 IHC, p16/Ki-67 DS and hTERC FISH amplification are all valid adjunctive biomarkers which significantly increase the sensitivity and specificity of cervical dysplasia diagnosis, especially when combined with HPV DNA testing. However, considering the global socioeconomic background, we can postulate that p16 and p16/ Ki-67 IHC can be used as a next step after positive cytology for ASC-US or LSIL specimens in low-income countries, instead of HPV DNA testing. Alternatively, if HPV DNA testing is covered by insurance, p16 or p16/Ki-67 DS and HPV DNA co-testing can be performed. In middle- and high-income countries, hTERC amplification can be performed as an adjunctive test to HPV DNA testing in women with ASC-US and LSIL. Full article

(This article belongs to the Special Issue Infection, Inflammation and Cancer)

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