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Cancer Signaling Pathways, Crosstalk and Therapeutics

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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 (31 August 2022) | Viewed by 37969

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Dr. Imran Khan

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Guest Editor

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
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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

Special Issue Information

Dear Colleagues,

Cancer is a major problem of disease worldwide and, each year, many millions of people are diagnosed with cancer around the world, and more than half of them die. Cancer ranks second, next to cardiovascular diseases, for causing the greatest number of deaths. Therefore, it is important to study cancer in depth. Cell death is an essential biological process in maintaining homeostasis, as well as in removing dead cells. Both cell growth and cell death are important mechanisms for cancer proliferation, development and for chemoresistance. Both mechanisms are complex, however, apoptosis, autophagy, necrosis, or necroptosis signaling cascade plays a crucial role. Moreover, tumor microenvironment has a significant impact on cell proliferation, death, metabolism and chemotherapy. Therefore, it is vital to consider all of these factors for chemotherapy. This Special Issue focuses on “Cancer Signaling Pathways, Crosstalk and Therapeutics”. The main objectives are not restricted to apoptosis, necrosis, autophagy, ferroptosis or lysosomal signaling cascade but also target various pathways for tumor annihilation, cell death for intrinsic and extrinsic apoptosis, novel plants, chemical drugs, nanomedicine or strategies targeting cancer promoting proteins (BH3, SMAC mimetics, cFLIP, XIAP).

This Special Issue welcomes the submission of original research and review articles focusing on cancer signaling pathways and therapeutics; however, research on new technologies employed for studying cancer biomarker identification, tracing cancer pathways, that will help us to understand cancer biology in depth is also welcome. This Special Issue will enlighten readers about new discoveries, advances, and development in cancer therapeutics.

Dr. Imran Khan
Dr. Faisal Aziz
Guest Editors

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Keywords

cancer biology
anticancer study
signaling pathway
apoptosis
autophagy
necrosis
necroptosis
nanomedicine

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Published Papers (13 papers)

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13 pages, 2814 KiB

Open AccessArticle

Brassinin Induces Apoptosis, Autophagy, and Paraptosis via MAPK Signaling Pathway Activation in Chronic Myelogenous Leukemia Cells

by Min Hee Yang, In Jin Ha, Seok-Geun Lee, Junhee Lee, Jae-Young Um, Gautam Sethi and Kwang Seok Ahn

Biology 2023, 12(2), 307; https://doi.org/10.3390/biology12020307 - 14 Feb 2023

Cited by 19 | Viewed by 2504

Abstract

Brassinin (BSN), a potent phytoalexin found in cruciferous vegetables, has been found to exhibit diverse anti-neoplastic effects on different cancers. However, the impact of BSN on chronic myelogenous leukemia (CML) cells and the possible mode of its actions have not been described earlier. We investigated the anti-cytotoxic effects of BSN on the KBM5, KCL22, K562, and LAMA84 CML cells and its underlying mechanisms of action in inducing programmed cell death. We noted that BSN could induce apoptosis, autophagy, and paraptosis in CML cells. BSN induced PARP cleavage, subG1 peak increase, and early apoptosis. The potential action of BSN on autophagy activation was confirmed by an LC3 expression and acridine orange assay. In addition, BSN induced paraptosis through increasing the reactive oxygen species (ROS) production, mitochondria damage, and endoplasmic reticulum (ER) stress. Moreover, BSN promoted the activation of the MAPK signaling pathway, and pharmacological inhibitors of this signaling pathway could alleviate all three forms of cell death induced by BSN. Our data indicated that BSN could initiate the activation of apoptosis, autophagy, and paraptosis through modulating the MAPK signaling pathway. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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16 pages, 2294 KiB

Open AccessArticle

Predicting Deleterious Non-Synonymous Single Nucleotide Polymorphisms (nsSNPs) of HRAS Gene and In Silico Evaluation of Their Structural and Functional Consequences towards Diagnosis and Prognosis of Cancer

by Chuan-Yu Chai, Sathiya Maran, Hin-Yee Thew, Yong-Chiang Tan, Nik Mohd Afizan Nik Abd Rahman, Wan-Hee Cheng, Kok-Song Lai, Jiun-Yan Loh and Wai-Sum Yap

Biology 2022, 11(11), 1604; https://doi.org/10.3390/biology11111604 - 2 Nov 2022

Cited by 7 | Viewed by 3140

Abstract

The Harvey rat sarcoma (HRAS) proto-oncogene belongs to the RAS family and is one of the pathogenic genes that cause cancer. Deleterious nsSNPs might have adverse consequences at the protein level. This study aimed to investigate deleterious nsSNPs in the HRAS gene in predicting structural alterations associated with mutants that disrupt normal protein–protein interactions. Functional and structural analysis was employed in analyzing the HRAS nsSNPs. Putative post-translational modification sites and the changes in protein–protein interactions, which included a variety of signal cascades, were also investigated. Five different bioinformatics tools predicted 33 nsSNPs as “pathogenic” or “harmful”. Stability analysis predicted rs1554885139, rs770492627, rs1589792804, rs730880460, rs104894227, rs104894227, and rs121917759 as unstable. Protein–protein interaction analysis revealed that HRAS has a hub connecting three clusters consisting of 11 proteins, and changes in HRAS might cause signal cascades to dissociate. Furthermore, Kaplan–Meier bioinformatics analyses indicated that the HRAS gene deregulation affected the overall survival rate of patients with breast cancer, leading to prognostic significance. Thus, based on these analyses, our study suggests that the reported nsSNPs of HRAS may serve as potential targets for different proteomic studies, diagnoses, and therapeutic interventions focusing on cancer. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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12 pages, 5217 KiB

Open AccessArticle

Identification of NRAS Downstream Genes with CRISPR Activation Screening

by Akiya Tatsumi, Haruka Hirakochi, Satomi Inoue, Yosuke Tanaka, Hidehiro Furuno, Masumi Ikeda, Sachiko Ishibashi, Towako Taguchi, Kouhei Yamamoto, Iichiroh Onishi, Zohar Sachs, David A. Largaespada, Masanobu Kitagawa and Morito Kurata

Biology 2022, 11(11), 1551; https://doi.org/10.3390/biology11111551 - 23 Oct 2022

Viewed by 2827

Abstract

Mutations in NRAS constitutively activate cell proliferation signaling in malignant neoplasms, such as leukemia and melanoma, and the clarification of comprehensive downstream genes of NRAS might lead to the control of cell-proliferative signals of NRAS-driven cancers. We previously established that NRAS expression and proliferative activity can be controlled with doxycycline and named as THP-1 B11. Using a CRISPR activation library on THP-1 B11 cells with the NRAS-off state, survival clones were harvested, and 21 candidate genes were identified. By inducting each candidate guide RNA with the CRISPR activation system, DOHH, HIST1H2AC, KRT32, and TAF6 showed higher cell-proliferative activity. The expression of DOHH, HIST1H2AC, and TAF6 was definitely upregulated with NRAS expression. Furthermore, MEK inhibitors resulted in the decreased expression of DOHH, HIST1H2AC, and TAF6 proteins in parental THP-1 cells. The knockdown of DOHH, HIST1H2AC, and TAF6 was found to reduce proliferation in THP-1 cells, indicating that they are involved in the downstream proliferation of NRAS. These molecules are expected to be new therapeutic targets for NRAS-mutant leukemia cells. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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19 pages, 8027 KiB

Open AccessArticle

Kinesin Eg5 Selective Inhibition by Newly Synthesized Molecules as an Alternative Approach to Counteract Breast Cancer Progression: An In Vitro Study

by Alessia Ricci, Amelia Cataldi, Simone Carradori and Susi Zara

Biology 2022, 11(10), 1450; https://doi.org/10.3390/biology11101450 - 2 Oct 2022

Cited by 3 | Viewed by 1857

Abstract

Breast cancer (BC) is one of the most diagnosed cancers in women. Recently, a promising target for BC treatment was found in kinesin Eg5, a mitotic motor protein that allows bipolar spindle formation and cell replication. Thus, the aim of this work was to evaluate the effects of novel thiadiazoline-based Eg5 inhibitors, analogs of K858, in an in vitro model of BC (MCF7 cell line). Compounds 2 and 41 were selected for their better profile as they reduce MCF7 viability at lower concentrations and with minimal effect on non-tumoral cells with respect to K858. Compounds 2 and 41 counteract MCF7 migration by negatively modulating the NF-kB/MMP-9 pathway. The expression of HIF-1α and VEGF appeared also reduced by 2 and 41 administration, thus preventing the recruitment of the molecular cascade involved in angiogenesis promotion. In addition, 2 provokes an increased caspase-3 activation thus triggering the MCF7 apoptotic event, while 41 and K858 seem to induce the necrosis axis, as disclosed by the increased expression of PARP. These results allow us to argue that 2 and 41 are able to simultaneously intervene on pivotal molecular signaling involved in breast cancer progression, leading to the assumption that Eg5 inhibition can represent a valid approach to counteract BC progression. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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17 pages, 3625 KiB

Open AccessArticle

Reelin Protects against Colon Pathology via p53 and May Be a Biomarker for Colon Cancer Progression

by José M. Serrano-Morales, María D. Vázquez-Carretero, Pablo García-Miranda, Ana E. Carvajal, María L. Calonge, Anunciación A. Ilundain and María J. Peral

Biology 2022, 11(10), 1406; https://doi.org/10.3390/biology11101406 - 26 Sep 2022

Cited by 2 | Viewed by 1871

Abstract

Previous observations made in human and mouse colons suggest that reelin protects the colon from pathology. In this study, we evaluated reelin expression during the transition from either colitis or precancerous lesions to colon cancer and tried to elucidate reelin regulation under these transition processes. Samples of healthy and pathological colons from humans and mice treated with either azoxymethane/dextran sulfate sodium (DSS) or azoxymethane alone were used. The relative abundances of reelin, DNMT-1 and ApoER2 mRNAs were determined by PCR in the colon samples cited above and in the tissue adjacent to mouse colon polyps and adenocarcinomas. In both, humans and mice, reelin mRNA abundance increased significantly in ulcerative colitis and slightly in polyps and decreased in adenomas and adenocarcinomas. Reelin expression was higher in the tissue adjacent to the colon adenocarcinoma and lower in the lesion itself. The reelin expression changes may result, at least in part, from those in DNMT-1 and appear to be independent of ApoER2. Lack of reelin downregulated p-Akt and p53 in healthy colon and prevented their increases in the inflamed colon, whereas it increased GSK-3β in DSS-untreated mice. In conclusion, reelin mRNA abundance depends on the severity of the colon pathology, and its upregulation in response to initial injuries might prevent the beginning of colon cancer, whereas reelin repression favors it. Increased p53 expression and activation may be involved in this protection. We also propose that changes in colon reelin abundance could be used to predict colon pathology progression. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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15 pages, 4803 KiB

Open AccessArticle

Downregulated ADAMTS1 Incorporating A2M Contributes to Tumorigenesis and Alters Tumor Immune Microenvironment in Lung Adenocarcinoma

by Hsiao-Chen Lee, Chao-Yuan Chang, Yung-Chi Huang, Kuan-Li Wu, Hung-Hsing Chiang, Yung-Yun Chang, Lian-Xiu Liu, Jen-Yu Hung, Ya-Ling Hsu, Yu-Yuan Wu and Ying-Ming Tsai

Biology 2022, 11(5), 760; https://doi.org/10.3390/biology11050760 - 16 May 2022

Cited by 4 | Viewed by 3299

Abstract

Lung adenocarcinoma (LUAD) still holds the most dreadful clinical outcomes worldwide. Despite advanced treatment strategies, there are still some unmet needs. Next-generation sequencing of large-scale cancer genomics discovery projects combined with bioinformatics provides the opportunity to take a step forward in meeting clinical conditions. Based on in-house and The Cancer Genome Atlas (TCGA) cohorts, the results showed decreased levels of ADAMTS1 conferred poor survival compared with normal parts. Gene set enrichment analyses (GSEA) indicated the negative correlation between ADAMTS1 and the potential roles of epithelial–mesenchymal transition (EMT), metastasis, and poor prognosis in LUAD patients. With the knockdown of ADAMTS1, A549 lung cancer cells exhibited more aggressive behaviors such as EMT and increased migration, resulting in cancer metastasis in a mouse model. The pathway interaction network disclosed the linkage of downregulated α2-macroglobulin (A2M), which regulates EMT and metastasis. Furthermore, immune components analysis indicated a positive relationship between ADAMTS1 and the infiltrating levels of multiple immune cells, especially anticancer CD4⁺ T cells in LUAD. Notably, ADAMTS1 expression was also inversely correlated with the accumulation of immunosuppressive myeloid-derived suppressor cells and regulatory T cells, implying the downregulated ADAMTS1 mediated immune adjustment to fit the tumor survival disadvantages in LUAD patients. In conclusion, our study indicates that ADAMTS1 interacts with A2M in regulating EMT and metastasis in LUAD. Additionally, ADAMTS1 contributes to poor prognosis and immune infiltration in LUAD patients Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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16 pages, 3074 KiB

Open AccessArticle

Leelamine Modulates STAT5 Pathway Causing Both Autophagy and Apoptosis in Chronic Myelogenous Leukemia Cells

by Young Yun Jung, Jae-Young Um, Arunachalam Chinnathambi, Chandramohan Govindasamy, Gautam Sethi and Kwang Seok Ahn

Biology 2022, 11(3), 366; https://doi.org/10.3390/biology11030366 - 25 Feb 2022

Cited by 11 | Viewed by 2465

Abstract

Leelamine (LEE) has recently attracted significant attention for its growth inhibitory effects against melanoma, breast cancer, and prostate cancer cells; however, its impact on hematological malignancies remains unclear. Here, we first investigate the cytotoxic effects of LEE on several human chronic myeloid leukemia (CML) cells. We noted that LEE stimulated both apoptosis and autophagy in CML cells. In addition, the constitutive activation of signal transducer and activator of transcription 5 (STAT5) was suppressed substantially upon LEE treatment. Moreover, STAT5 knockdown with small interfering RNA (siRNA) increased LEE-induced apoptosis as well as autophagy and affected the levels of various oncogenic proteins. Thus, the targeted mitigation of STAT5 activation by LEE can contribute to its diverse anticancer effects by enhancing two distinct cell death pathways. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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18 pages, 4728 KiB

Open AccessArticle

TERT Promoter Revertant Mutation Inhibits Melanoma Growth through Intrinsic Apoptosis

by Yanbing Wang, Yiwu Chen, Chang Li, Zhiwei Xiao, Hongming Yuan, Yuanzhu Zhang, Daxin Pang, Xiaochun Tang, Mengjing Li and Hongsheng Ouyang

Biology 2022, 11(1), 141; https://doi.org/10.3390/biology11010141 - 14 Jan 2022

Cited by 5 | Viewed by 3342 | Correction

Abstract

Human telomerase is a specialized DNA polymerase whose catalytic core includes both TERT and human telomerase RNA (hTR). Telomerase in humans, which is silent in most somatic cells, is activated to maintain the telomere length (TEL) in various types of cancer cells, including melanoma. In the vast majority of tumor cells, the TERT promoter is mutated to promote proliferation and inhibit apoptosis. Here, we exploited NG-ABEmax to revert TERT -146 T to -146 C in melanoma, and successfully obtained TERT promoter revertant mutant cells. These TERT revertant mutant cells exhibited significant growth inhibition both in vitro and in vivo. Moreover, A375^−146C/C cells exhibited telomere shortening and the downregulation of TERT at both the transcription and protein levels, and migration and invasion were inhibited. In addition, TERT promoter revertant mutation abrogated the inhibitory effect of mutant TERT on apoptosis via B-cell lymphoma 2 (Bcl-2), ultimately leading to cell death. Collectively, the results of our work demonstrate that reverting mutations in the TERT promoter is a potential therapeutic option for melanoma. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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15 pages, 3479 KiB

Open AccessArticle

3-Formylchromone Counteracts STAT3 Signaling Pathway by Elevating SHP-2 Expression in Hepatocellular Carcinoma

by Chakrabhavi Dhananjaya Mohan, Min Hee Yang, Shobith Rangappa, Arunachalam Chinnathambi, Sulaiman Ali Alharbi, Tahani Awad Alahmadi, Amudha Deivasigamani, Kam Man Hui, Gautam Sethi, Kanchugarakoppal S. Rangappa and Kwang Seok Ahn

Biology 2022, 11(1), 29; https://doi.org/10.3390/biology11010029 - 26 Dec 2021

Cited by 21 | Viewed by 3910

Abstract

Hepatocellular carcinoma (HCC) is one of the leading cancers that contribute to a large number of deaths throughout the globe. The signal transducer and activator of transcription 3 (STAT3) is a tumorigenic protein that is overactivated in several human malignancies including HCC. In the present report, the effect of 3-formylchromone (3FC) on the STAT3 signaling pathway in the HCC model was investigated. 3FC downregulated the constitutive phosphorylation of STAT3 and non-receptor tyrosine kinases such as JAK1 and JAK2. It also suppressed the transportation of STAT3 to the nucleus and reduced its DNA-binding ability. Pervanadate treatment overrode the 3FC-triggered STAT3 inhibition, and the profiling of cellular phosphatase expression revealed an increase in SHP-2 levels upon 3FC treatment. The siRNA-driven deletion of SHP-2 led to reinstate STAT3 activation. 3FC downmodulated the levels of various oncogenic proteins and decreased CXCL12-driven cell migration and invasion. Interestingly, 3FC did not exhibit any substantial toxicity, whereas it significantly regressed tumor growth in an orthotopic HCC mouse model and abrogated lung metastasis. Overall, 3FC can function as a potent agent that can display antitumor activity by targeting STAT3 signaling in HCC models. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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17 pages, 4402 KiB

Open AccessArticle

Mechanism of Ca²⁺-Dependent Pro-Apoptotic Action of Selenium Nanoparticles, Mediated by Activation of Cx43 Hemichannels

by Egor A. Turovsky and Elena G. Varlamova

Biology 2021, 10(8), 743; https://doi.org/10.3390/biology10080743 - 3 Aug 2021

Cited by 33 | Viewed by 2983

Abstract

To date, there are practically no data on the mechanisms of the selenium nanoparticles action on calcium homeostasis, intracellular signaling in cancer cells, and on the relationship of signaling pathways activated by an increase in Ca²⁺ in the cytosol with the induction of apoptosis, which is of great importance. The study of these mechanisms is important for understanding the cytotoxic effect of selenium nanoparticles and the role of this microelement in the regulation of carcinogenesis. The work is devoted to the study of the role of selenium nanoparticles obtained by laser ablation in the activation of the calcium signaling system and the induction of apoptosis in human glioblastoma cells (A-172 cell line). In this work, it was shown for the first time that the generation of Ca²⁺ signals in A-172 cells occurs in response to the application of various concentrations of selenium nanoparticles. The intracellular mechanism responsible for the generation of these Ca²⁺ signals has also been established. It was found that nanoparticles promote the mobilization of Ca²⁺ ions from the endoplasmic reticulum through the IP₃-receptor. This leads to the activation of vesicular release of ATP through connexin hemichannels (Cx43) and paracrine cell activation through purinergic receptors (mainly P2Y). In addition, it was shown that the activation of this signaling pathway is accompanied by an increase in the expression of pro-apoptotic genes and the induction of apoptosis. For the first time, the role of Cx43 in the regulation of apoptosis caused by selenium nanoparticles in glioblastoma cells has been shown. It was found that inhibition of Cx43 leads to a significant suppression of the induction of apoptosis in these cells after 24 h treatment of cells with selenium nanoparticles at a concentration of 5 µg/mL. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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Review

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19 pages, 2927 KiB

Open AccessReview

Target Therapy for Hepatocellular Carcinoma: Beyond Receptor Tyrosine Kinase Inhibitors and Immune Checkpoint Inhibitors

by Hyunjung Park, Hyerin Park, Jiyeon Baek, Hyuk Moon and Simon Weonsang Ro

Biology 2022, 11(4), 585; https://doi.org/10.3390/biology11040585 - 12 Apr 2022

Cited by 9 | Viewed by 2985

Abstract

Hepatocellular carcinoma (HCC) is a major health concern worldwide, and its incidence is increasing steadily. To date, receptor tyrosine kinases (RTKs) are the most favored molecular targets for the treatment of HCC, followed by immune checkpoint regulators such as PD-1, PD-L1, and CTLA-4. With less than desirable clinical outcomes from RTK inhibitors as well as immune checkpoint inhibitors (ICI) so far, novel molecular target therapies have been proposed for HCC. In this review, we will introduce diverse molecular signaling pathways that are aberrantly activated in HCC, focusing on YAP/TAZ, Hedgehog, and Wnt/β-catenin signaling pathways, and discuss potential therapeutic strategies targeting the signaling pathways in HCC. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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14 pages, 768 KiB

Open AccessReview

Relevance of miR-223 as Potential Diagnostic and Prognostic Markers in Cancer

by Faisal Aziz, Abhijit Chakraborty, Imran Khan and Josh Monts

Biology 2022, 11(2), 249; https://doi.org/10.3390/biology11020249 - 6 Feb 2022

Cited by 17 | Viewed by 3948

Abstract

In 1993, the discovery of microRNAs in Caenorhabditis elegans (C. elegans) altered the paradigmatic view of RNA biology and post-transcriptional gene regulation. Further study revealed the role of microRNAs in disease development and progression. In particular, this review highlights microRNA-223 (miR-223 or miRNA-223) expression in malignant neoplastic disorders. miR-223 expression controls aspects of hematopoiesis and apoptosis, and cell proliferation, migration, and invasion. miR-223 regulates a number of gene targets, including cytoplasmic activation/proliferation-associated protein-1 (Caprin-1), insulin-like growth factor-1 receptor (IGF-1R), and other cell proliferation- and cell cycle-associated genes. Several studies have proposed miR-223 as a novel biomarker for early cancer diagnosis. Here, we emphasize miR-223′s role in the development and progression of cancer. Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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Other

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2 pages, 755 KiB

Open AccessCorrection

Correction: Wang et al. TERT Promoter Revertant Mutation Inhibits Melanoma Growth through Intrinsic Apoptosis. Biology 2022, 11, 141

by Yanbing Wang, Yiwu Chen, Chang Li, Zhiwei Xiao, Hongming Yuan, Yuanzhu Zhang, Daxin Pang, Xiaochun Tang, Mengjing Li and Hongsheng Ouyang

Biology 2022, 11(10), 1400; https://doi.org/10.3390/biology11101400 - 26 Sep 2022

Viewed by 1085

Abstract

The authors would like to make the following correction to the published paper [...] Full article

(This article belongs to the Special Issue Cancer Signaling Pathways, Crosstalk and Therapeutics)

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