Advance in Tumorigenesis Research and Cancer Cell Therapy

Topic Information

Dear Colleagues,

Cancer is still the leading cause of human disease-related death worldwide. Although the application of molecular targeting therapy and immune checkpoint inhibitors has greatly improved patients’ outcome, the five-year overall survival rate is still unsatisfactory for patients with cancer. Hence, there is an urgent need to better understand the molecular mechanisms of cancer occurrence and progression, thereby improving the diagnostics and developing novel therapeutic approaches. Over the past few decades, breakthroughs in gene engineering and editing technologies have led to the fast improvement of chimeric antigen receptor (CAR)-T therapy. CAR-T cell therapies have achieved great success for treating hematological malignancies. However, their application is limited in solid tumors owing to antigen loss and mutation, physical barriers, and an immunosuppressive tumor microenvironment. To overcome the challenges of CAR-T cells, increasing efforts are focused on developing CAR-T to expand its applied ranges. This Special Issue will highlight the latest advances in research on tumorigenesis and cancer progression, as well as the advancements of CAR engineering for solid tumors, which will cover both basic and clinical aspects that advance our understanding of human cancer.

Prof. Dr. Ming Sun
Dr. Xianghua Liu
Dr. Xuefei Shi
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biology biology	3.6	5.7	2012	16.4 Days	CHF 2700
Cancers cancers	4.5	8.0	2009	17.4 Days	CHF 2900

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Published Papers (11 papers)

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Open AccessArticle

The Clinical Significance of Circulating Lymphocytes Morphology in Diffuse Large B-Cell Lymphoma As Determined by a Novel, Highly Sensitive Microscopy

by Gil Fridberg, Galit Horn, Anat Globerson Levin, Dan Benisty, Sigi Kay, Chen Glait-Santar, Chava Perry, Ron Ram, Irit Avivi and Ben-Zion Katz

Cancers 2023, 15(23), 5611; https://doi.org/10.3390/cancers15235611 - 28 Nov 2023

Cited by 2 | Viewed by 2948

Abstract

Chimeric Antigen Receptor T-cell (CAR T) therapy has become the preferable treatment in relapsed/refractory diffuse large B-cell lymphomas (DLBCL) patients. Detection of CAR Ts in peripheral blood smear (PBS) is challenging due to insufficient data regarding their morphology and low sensitivity. The morphological [...] Read more.

Chimeric Antigen Receptor T-cell (CAR T) therapy has become the preferable treatment in relapsed/refractory diffuse large B-cell lymphomas (DLBCL) patients. Detection of CAR Ts in peripheral blood smear (PBS) is challenging due to insufficient data regarding their morphology and low sensitivity. The morphological evolution of CAR Ts along their production process, and in patients, was established by Full-Field Morphology (FFM), a novel digital microscopy approach that provides highly sensitive PBS analysis. At day 8 of production, 42.7 ± 10.8% of the CAR T transduced cells exhibited activated morphology compared with 9.3 ± 3.8% in untransduced cells. Moreover, engagement of transduced CAR Ts with target cells resulted in further morphological transformation into activated morphology (83 ± 5.6% of the cells). In patients, the average number of day 5 CAR Ts, and their sustained presence, were significantly higher in patients obtaining complete response. A high number of activated morphology CAR Ts at day 14 was associated with prolonged cytokine release storm. Overall, CAR Ts exhibited heterogeneous morphology, with the activated morphology attributed predominantly to transduced cells following engagement with target cells. Post-transfusion CAR T detection was associated with increased complete responses. FFM CAR T surveillance in PBS may serve as a simple inexpensive method to provide clinically relevant insights into this treatment modality. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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Supplementary File 1 (ZIP, 1138 KiB)

16 pages, 1592 KiB  

Open AccessArticle

USP53 Exerts Tumor-Promoting Effects in Triple-Negative Breast Cancer by Deubiquitinating CRKL

by Yi Liu, Wei Tang and Feng Yao

Cancers 2023, 15(20), 5033; https://doi.org/10.3390/cancers15205033 - 18 Oct 2023

Cited by 3 | Viewed by 1663

Abstract

Breast cancer (BC) ranks in the top five malignant tumors in terms of morbidity and mortality rates. Among BC subtypes, TNBC has a high recurrence rate and metastasis rate and the worst prognosis. However, the exact mechanism by which TNBC develops is unclear. [...] Read more.

Breast cancer (BC) ranks in the top five malignant tumors in terms of morbidity and mortality rates. Among BC subtypes, TNBC has a high recurrence rate and metastasis rate and the worst prognosis. However, the exact mechanism by which TNBC develops is unclear. Here, we show that the deubiquitinase USP53 contributes to tumor growth and metastasis in TNBC. USP53 is overexpressed in TNBC, and this phenotype is linked to a poor prognosis. Functionally, USP53 promotes TNBC cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT). More importantly, USP53 decreases the chemosensitivity of BC cells by enhancing v-crk sarcoma virus CT10 oncogene homologue (avian)-like (CRKL) expression. Mechanistically, USP53 directly binds CRKL to stabilize and deubiquitinate it, thereby preventing CRKL degradation. Overall, we discovered that USP53 deubiquitinates CRKL, encourages tumor development and metastasis, and reduces chemosensitivity in TNBC. These findings imply that USP53 might represent a new therapeutic target for the treatment of TNBC. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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15 pages, 2930 KiB  

Open AccessReview

The Multifaceted Functions of Prion Protein (PrP^C) in Cancer

by Roland Abi Nahed, Hasan Safwan-Zaiter, Kevin Gemy, Camille Lyko, Mélanie Boudaud, Morgane Desseux, Christel Marquette, Tiphaine Barjat, Nadia Alfaidy and Mohamed Benharouga

Cancers 2023, 15(20), 4982; https://doi.org/10.3390/cancers15204982 - 13 Oct 2023

Cited by 5 | Viewed by 3754

Abstract

The cellular prion protein (PrP^C) is a glycoprotein anchored to the cell surface by glycosylphosphatidylinositol (GPI). PrP^C is expressed both in the brain and in peripheral tissues. Investigations on PrP^C’s functions revealed its direct involvement in neurodegenerative and [...] Read more.

The cellular prion protein (PrP^C) is a glycoprotein anchored to the cell surface by glycosylphosphatidylinositol (GPI). PrP^C is expressed both in the brain and in peripheral tissues. Investigations on PrP^C’s functions revealed its direct involvement in neurodegenerative and prion diseases, as well as in various physiological processes such as anti-oxidative functions, copper homeostasis, trans-membrane signaling, and cell adhesion. Recent findings have revealed the ectopic expression of PrP^C in various cancers including gastric, melanoma, breast, colorectal, pancreatic, as well as rare cancers, where PrP^C promotes cellular migration and invasion, tumor growth, and metastasis. Through its downstream signaling, PrP^C has also been reported to be involved in resistance to chemotherapy and tumor cell apoptosis. This review summarizes the variance of expression of PrP^C in different types of cancers and discusses its roles in their development and progression, as well as its use as a potential target to treat such cancers. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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19 pages, 1705 KiB  

Open AccessArticle

Selective Activation of M₁ Muscarinic Receptors Attenuates Human Colon Cancer Cell Proliferation

by Margaret H. Sundel, Natalia Sampaio Moura, Kunrong Cheng, Oscar Chatain, Shien Hu, Cinthia B. Drachenberg, Guofeng Xie and Jean-Pierre Raufman

Cancers 2023, 15(19), 4766; https://doi.org/10.3390/cancers15194766 - 28 Sep 2023

Cited by 1 | Viewed by 1635

Abstract

M₃ muscarinic receptor (M₃R) activation stimulates colon cancer cell proliferation, migration, and invasion; M₃R expression is augmented in colon cancer and ablating M₃R expression in mice attenuates colon neoplasia. Several lines of investigation suggest that in [...] Read more.

M₃ muscarinic receptor (M₃R) activation stimulates colon cancer cell proliferation, migration, and invasion; M₃R expression is augmented in colon cancer and ablating M₃R expression in mice attenuates colon neoplasia. Several lines of investigation suggest that in contrast to these pro-neoplastic effects of M₃R, M₁R plays an opposite role, protecting colon epithelial cells against neoplastic transformation. To pursue these intriguing findings, we examined the relative expression of M₁R versus M₃R in progressive stages of colon neoplasia and the effect of treating colon cancer cells with selective M₁R agonists. We detected divergent expression of M₁R and M₃R in progressive colon neoplasia, from aberrant crypt foci to adenomas, primary colon cancers, and colon cancer metastases. Treating three human colon cancer cell lines with two selective M₁R agonists, we found that in contrast to the effects of M₃R activation, selective activation of M₁R reversibly inhibited cell proliferation. Moreover, these effects were diminished by pre-incubating cells with a selective M₁R inhibitor. Mechanistic insights were gained using selective chemical inhibitors of post-muscarinic receptor signaling molecules and immunoblotting to demonstrate M₁R-dependent changes in the activation (phosphorylation) of key downstream kinases, EGFR, ERK1/2, and p38 MAPK. We did not detect a role for drug toxicity, cellular senescence, or apoptosis in mediating M₁R agonist-induced attenuated cell proliferation. Lastly, adding M₁R-selective agonists to colon cancer cells augmented the anti-proliferative effects of conventional chemotherapeutic agents. Collectively, these results suggest that selective M₁R agonism for advanced colon cancer, alone or in combination with conventional chemotherapy, is a therapeutic strategy worth exploring. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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13 pages, 597 KiB  

Open AccessReview

Type IV P-Type ATPases: Recent Updates in Cancer Development, Progression, and Treatment

by Eugenia M. Yazlovitskaya and Todd R. Graham

Cancers 2023, 15(17), 4327; https://doi.org/10.3390/cancers15174327 - 30 Aug 2023

Cited by 3 | Viewed by 2085

Abstract

Adaptations of cancer cells for survival are remarkable. One of the most significant properties of cancer cells to prevent the immune system response and resist chemotherapy is the altered lipid metabolism and resulting irregular cell membrane composition. The phospholipid distribution in the plasma [...] Read more.

Adaptations of cancer cells for survival are remarkable. One of the most significant properties of cancer cells to prevent the immune system response and resist chemotherapy is the altered lipid metabolism and resulting irregular cell membrane composition. The phospholipid distribution in the plasma membrane of normal animal cells is distinctly asymmetric. Lipid flippases are a family of enzymes regulating membrane asymmetry, and the main class of flippases are type IV P-type ATPases (P4-ATPases). Alteration in the function of flippases results in changes to membrane organization. For some lipids, such as phosphatidylserine, the changes are so drastic that they are considered cancer biomarkers. This review will analyze and discuss recent publications highlighting the role that P4-ATPases play in the development and progression of various cancer types, as well as prospects of targeting P4-ATPases for anti-cancer treatment. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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26 pages, 5484 KiB  

Open AccessArticle

The Putative S1PR1 Modulator ACT-209905 Impairs Growth and Migration of Glioblastoma Cells In Vitro

by Sandra Bien-Möller, Fan Chen, Yong Xiao, Hanjo Köppe, Gabriele Jedlitschky, Ulrike Meyer, Céline Tolksdorf, Markus Grube, Sascha Marx, Mladen V. Tzvetkov, Henry W. S. Schroeder and Bernhard H. Rauch

Cancers 2023, 15(17), 4273; https://doi.org/10.3390/cancers15174273 - 26 Aug 2023

Cited by 2 | Viewed by 1761

Abstract

Glioblastoma (GBM) is still a deadly tumor due to its highly infiltrative growth behavior and its resistance to therapy. Evidence is accumulating that sphingosine-1-phosphate (S1P) acts as an important tumor-promoting molecule that is involved in the activation of the S1P receptor subtype 1 [...] Read more.

Glioblastoma (GBM) is still a deadly tumor due to its highly infiltrative growth behavior and its resistance to therapy. Evidence is accumulating that sphingosine-1-phosphate (S1P) acts as an important tumor-promoting molecule that is involved in the activation of the S1P receptor subtype 1 (S1PR1). Therefore, we investigated the effect of ACT-209905 (a putative S1PR1 modulator) on the growth of human (primary cells, LN-18) and murine (GL261) GBM cells. The viability and migration of GBM cells were both reduced by ACT-209905. Furthermore, co-culture with monocytic THP-1 cells or conditioned medium enhanced the viability and migration of GBM cells, suggesting that THP-1 cells secrete factors which stimulate GBM cell growth. ACT-209905 inhibited the THP-1-induced enhancement of GBM cell growth and migration. Immunoblot analyses showed that ACT-209905 reduced the activation of growth-promoting kinases (p38, AKT1 and ERK1/2), whereas THP-1 cells and conditioned medium caused an activation of these kinases. In addition, ACT-209905 diminished the surface expression of pro-migratory molecules and reduced CD62P-positive GBM cells. In contrast, THP-1 cells increased the ICAM-1 and P-Selectin content of GBM cells which was reversed by ACT-209905. In conclusion, our study suggests the role of S1PR1 signaling in the growth of GBM cells and gives a partial explanation for the pro-tumorigenic effects that macrophages might have on GBM cells. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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31 pages, 1705 KiB  

Open AccessReview

Mutant IDH in Gliomas: Role in Cancer and Treatment Options

by Georgios Solomou, Alina Finch, Asim Asghar and Chiara Bardella

Cancers 2023, 15(11), 2883; https://doi.org/10.3390/cancers15112883 - 23 May 2023

Cited by 20 | Viewed by 5771

Abstract

Altered metabolism is a common feature of many cancers and, in some cases, is a consequence of mutation in metabolic genes, such as the ones involved in the TCA cycle. Isocitrate dehydrogenase (IDH) is mutated in many gliomas and other cancers. [...] Read more.

Altered metabolism is a common feature of many cancers and, in some cases, is a consequence of mutation in metabolic genes, such as the ones involved in the TCA cycle. Isocitrate dehydrogenase (IDH) is mutated in many gliomas and other cancers. Physiologically, IDH converts isocitrate to α-ketoglutarate (α-KG), but when mutated, IDH reduces α-KG to D2-hydroxyglutarate (D2-HG). D2-HG accumulates at elevated levels in IDH mutant tumours, and in the last decade, a massive effort has been made to develop small inhibitors targeting mutant IDH. In this review, we summarise the current knowledge about the cellular and molecular consequences of IDH mutations and the therapeutic approaches developed to target IDH mutant tumours, focusing on gliomas. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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17 pages, 1889 KiB  

Open AccessReview

Regulatory Mechanisms and Reversal of CD8⁺T Cell Exhaustion: A Literature Review

by Wanwan Zhu, Yiming Li, Mingwei Han and Jianli Jiang

Biology 2023, 12(4), 541; https://doi.org/10.3390/biology12040541 - 1 Apr 2023

Cited by 16 | Viewed by 9931

Abstract

CD8⁺T cell exhaustion is a state of T cell dysfunction during chronic infection and tumor progression. Exhausted CD8⁺T cells are characterized by low effector function, high expression of inhibitory receptors, unique metabolic patterns, and altered transcriptional profiles. Recently, advances [...] Read more.

CD8⁺T cell exhaustion is a state of T cell dysfunction during chronic infection and tumor progression. Exhausted CD8⁺T cells are characterized by low effector function, high expression of inhibitory receptors, unique metabolic patterns, and altered transcriptional profiles. Recently, advances in understanding and interfering with the regulatory mechanisms associated with T cell exhaustion in tumor immunotherapy have brought greater attention to the field. Therefore, we emphasize the typical features and related mechanisms of CD8⁺T cell exhaustion and particularly the potential for its reversal, which has clinical implications for immunotherapy. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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20 pages, 2922 KiB  

Open AccessArticle

FGFR2c Upregulation Contributes to Cancer-Associated Fibroblast Program Activation and to Enhanced Autophagy in Actinic Keratosis-Derived Dermal Fibroblasts: A Possible Role in Precancerous Cell/Stromal Cell Crosstalk

by Luisa Guttieri, Salvatore Raffa, Gerardo Salerno, Rachele Bigi, Flavia Persechino, Vincenzo Visco, Maria Rosaria Torrisi, Danilo Ranieri and Francesca Belleudi

Biology 2023, 12(3), 463; https://doi.org/10.3390/biology12030463 - 16 Mar 2023

Cited by 3 | Viewed by 2265

Abstract

Actinic keratosis (AK) is a preneoplastic skin disorder which can rapidly progress to cutaneous squamous cell carcinomas (SCCs). In light of our previous findings, indicating a possible oncogenic role of the mesenchymal isoform of FGFR2 (FGFR2c) aberrantly expressed in AK keratinocytes, we analyzed [...] Read more.

Actinic keratosis (AK) is a preneoplastic skin disorder which can rapidly progress to cutaneous squamous cell carcinomas (SCCs). In light of our previous findings, indicating a possible oncogenic role of the mesenchymal isoform of FGFR2 (FGFR2c) aberrantly expressed in AK keratinocytes, we analyzed the possible tumor-promoting role of this receptor in the stromal AK counterpart in this work. Molecular analysis showed that, particularly in early AK lesions, FGFR2c dermal upregulation is accompanied by the downregulation of the cancer-associated fibroblasts (CAF) transcription repressor CSL, the upregulation of the CAF activator ULK3, and the consequent CAF gene induction. Immunofluorescence and molecular analysis, coupled with silencing approaches by siRNA, applied on primary cultures of KIN I-derived fibroblasts, indicated that FGFR2c upregulation contribute to CAF signature and the increased autophagy in response to FGF2. Magnetic bead-based multiplex assay, combined with FGFR2 signaling shut-off approaches, indicated that, especially in response to FGF2, IL-6 secretion could depend on FGFR2c high expression and signaling, suggesting the possible establishment of FGFR2c-dependent secretory autophagy, contributing to tumor-promoting factor release. Overall, our results identified FGFR2c as a signaling molecule involved in controlling precancerous/stromal cell oncogenic crosstalk, pointing to this receptor as a possible early molecular marker predictive for AK’s rapid malignant progression. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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17 pages, 9083 KiB  

Open AccessArticle

KIF2C Facilitates Tumor Growth and Metastasis in Pancreatic Ductal Adenocarcinoma

by Xing Huang, Feng Zhao, Quan Wu, Zitong Wang, Haiyue Ren, Qiqi Zhang, Zhe Wang and Jin Xu

Cancers 2023, 15(5), 1502; https://doi.org/10.3390/cancers15051502 - 27 Feb 2023

Cited by 11 | Viewed by 2410

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer with a poor prognosis. For PDAC, an increase in the survival time of patients and a reduction mortality have not yet successfully been achieved. In many research works, Kinesin family member 2C (KIF2C) is [...] Read more.

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer with a poor prognosis. For PDAC, an increase in the survival time of patients and a reduction mortality have not yet successfully been achieved. In many research works, Kinesin family member 2C (KIF2C) is highly expressed in several tumors. Nevertheless, the role of KIF2C in pancreatic cancer is unknown. In this study, we found that KIF2C expression is significantly upregulated in human PDAC tissues and cell lines such as ASPC-1 and MIA-PaCa2. Moreover, KIF2C upregulation is associated with a poor prognosis when combining the expression of KIF2C with clinical information. Through cell functional assays and the construction of animal models, we showed that KIF2C promotes PDAC cell proliferation, migration, invasion, and metastasis, both in vitro and in vivo. Finally, the results of sequencing showed that the overexpression of KIF2C causes a decrease in some proinflammatory factors and chemokines. The cell cycle detection indicated that the pancreatic cancer cells in the overexpressed group had abnormal proliferation in the G2 and S phases. These results revealed the potential of KIF2C as a therapeutic target for the treatment of PDAC. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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19 pages, 962 KiB  

Open AccessReview

The Role of CXC Chemokines in Cancer Progression

by Tiantian Wu, Wannian Yang, Aiqin Sun, Zhixiao Wei and Qiong Lin

Cancers 2023, 15(1), 167; https://doi.org/10.3390/cancers15010167 - 28 Dec 2022

Cited by 44 | Viewed by 4167

Abstract

CXC chemokines are small chemotactic and secreted cytokines. Studies have shown that CXC chemokines are dysregulated in multiple types of cancer and are closely correlated with tumor progression. The CXC chemokine family has a dual function in tumor development, either tumor-promoting or tumor-suppressive [...] Read more.

CXC chemokines are small chemotactic and secreted cytokines. Studies have shown that CXC chemokines are dysregulated in multiple types of cancer and are closely correlated with tumor progression. The CXC chemokine family has a dual function in tumor development, either tumor-promoting or tumor-suppressive depending on the context of cellular signaling. Recent evidence highlights the pro-tumorigenic properties of CXC chemokines in most human cancers. CXC chemokines were found to play pivotal roles in promoting angiogenesis, stimulating inflammatory responses, and facilitating tumor metastases. Enhanced expression of CXC chemokines is always signatured with inferior survival and prognosis. The levels of CXC chemokines in cancer patients are in dynamic change according to the tumor contexts (e.g., chemotherapy resistance and tumor recurrence after surgery). Thus, CXC chemokines have great potential to be used as diagnostic and prognostic biomarkers and therapeutic targets. Currently, the molecular mechanisms underlying the effect of CXC chemokines on tumor inflammation and metastasis remain unclear and application of antagonists and neutralizing antibodies of CXC chemokines signaling for cancer therapy is still not fully established. This article will review the roles of CXC chemokines in promoting tumorigenesis and progression and address the future research directions of CXC chemokines for cancer treatment. Full article

(This article belongs to the Topic Advance in Tumorigenesis Research and Cancer Cell Therapy)

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