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Future Challenges of Targeted Therapy of Cancers

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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 (30 September 2023) | Viewed by 5071

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Special Issue Editor

Prof. Dr. Simona Gurzu

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Guest Editor

Department of Pathology, George Emil Palade University of Medicine, Pharmacy, Sciences and Technology, 38 Gheorghe Marinescu Street, 540139 Targu Mures, Romania
Interests: oncopathology; gastric cancer; colorectal cancer; hepatocellular carcinoma; epithelial–mesenchymal transition; targeted therapy of cancer; histopathology; molecular pathology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The scope of this Special Issue is to collect papers referring to updates in the targeted therapy of cancers. As future individualized therapy is predicted to be mainly based on gene profile, the genetic background should be more deeply understood, from cell lines to circulating tumor cells and tissue biomarkers. Data concerning the heterogeneity of tumors and a deeply understanding of their environment could also have a therapeutic impact. Any research or review papers which may have implications in improving oncologic therapy are welcome, and we encourage the presentation of clinical trial results. If some papers are mainly based on in silico analyses or the examination of public gene databases, they should include an external validation of their own cohort.

You may choose our Joint Special Issue in CIMB.

Prof. Dr. Simona Gurzu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

biomarkers
tumor tissue
individualized therapy
gene profile
epithelial–mesenchymal transition
immunotherapy
angiogenesis
metastases
oncology
pathology

Published Papers (3 papers)

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Research

13 pages, 3231 KiB

Open AccessArticle

Mucin-Phenotype and Expression of the Protein V-Set and Immunoglobulin Domain Containing 1 (VSIG1): New Insights into Gastric Carcinogenesis

by Catalin-Bogdan Satala, Ioan Jung and Simona Gurzu

Int. J. Mol. Sci. 2023, 24(10), 8697; https://doi.org/10.3390/ijms24108697 - 12 May 2023

Viewed by 1096

Abstract

In gastric cancer (GC), intestinal metaplasia (IM) is a common precursor lesion, but its relationship to the MUC2/MUC5AC/CDX2 axis is not completely understood. Although V-set and immunoglobulin domain containing 1 (VSIG1) is supposed to be a specific marker for gastric mucosa and GC, respectively, no data about its relationship with IM or mucin phenotype have been published. The aim of our study was to explore the possible linkage between IM and these four molecules. The clinicopathological features of 60 randomly selected GCs were examined in association with VSIG1, MUC2, MUC5AC and CDX2. Two online database platforms were also used to establish the transcription factors (TFs) network involved in MUC2/MUC5AC/CDX2 cascade. IM was more frequently encountered in females (11/16 cases) and in patients below 60 years old (10/16 cases). Poorly differentiated (G3) carcinomas tended to show a loss of CDX2 (27/33 cases) but not of MUC2 and MUC5AC. MUC5AC and CDX2 were lost in parallel with the depth of invasion of the pT4 stage (28/35 and 29/35 cases), while an advanced Dukes-MAC-like stage was only correlated with CDX2 and VSIG1 loss (20/37 and 30/37 cases). VSIG1 was directly correlated with MUC5AC (p = 0.04) as an indicator of gastric phenotype. MUC2-negative cases showed a propensity towards lymphatic invasion (37/40 cases) and distant metastases, while CDX2-negative cases tended to associate with hematogenous dissemination (30/40 cases). Regarding the molecular network, only 3 of the 19 TFs involved in this carcinogenic cascade (SP1, RELA, NFKB1) interacted with all targeted genes. In GC, VSIG1 can be considered an indicator of gastric phenotype carcinomas, where carcinogenesis is mainly driven by MUC5AC. Although infrequently encountered in GC, CDX2 positivity might indicate a locally advanced stage and risk for vascular invasion, especially in tumors developed against the background of IM. The loss of VSIG1 indicates a risk for lymph node metastases. Full article

(This article belongs to the Special Issue Future Challenges of Targeted Therapy of Cancers)

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17 pages, 2778 KiB

Open AccessArticle

The Effect of Silencing the Genes Responsible for the Level of Sphingosine-1-phosphate on the Apoptosis of Colon Cancer Cells

by Adam R. Markowski, Arkadiusz Żbikowski, Piotr Zabielski, Urszula Chlabicz, Patrycja Sadowska, Karolina Pogodzińska and Agnieszka U. Błachnio-Zabielska

Int. J. Mol. Sci. 2023, 24(8), 7197; https://doi.org/10.3390/ijms24087197 - 13 Apr 2023

Cited by 2 | Viewed by 1512

Abstract

Sphingosine-1-phosphate (S1P) and ceramides (Cer) are engaged in key events of signal transduction, but their involvement in the pathogenesis of colorectal cancer is not conclusive. The aim of our study was to investigate how the modulation of sphingolipid metabolism through the silencing of the genes involved in the formation (SPHK1) and degradation (SGPL1) of sphingosine-1-phosphate would affect the sphingolipid profile and apoptosis of HCT-116 human colorectal cancer cells. Silencing of SPHK1 expression decreased S1P content in HCT-116 cells, which was accompanied by an elevation in sphingosine, C18:0-Cer, and C18:1-Cer, increase in the expression and activation of Caspase-3 and -9, and augmentation of apoptosis. Interestingly, silencing of SGLP1 expression increased cellular content of both the S1P and Cer (C16:0-; C18:0-; C18:1-; C20:0-; and C22:0-Cer), yet inhibited activation of Caspase-3 and upregulated protein expression of Cathepsin-D. The above findings suggest that modulation of the S1P level and S1P/Cer ratio regulates both cellular apoptosis and CRC metastasis through Cathepsin-D modulation. The cellular ratio of S1P/Cer seems to be a crucial component of the above mechanism. Full article

(This article belongs to the Special Issue Future Challenges of Targeted Therapy of Cancers)

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12 pages, 5779 KiB

Open AccessArticle

TNF−α Secreted from Macrophages Increases the Expression of Prometastatic Integrin αV in Gastric Cancer

by Mi-Aie Hwang, Misun Won, Joo-Young Im, Mi-Jung Kang, Dae-Hyuk Kweon and Bo-Kyung Kim

Int. J. Mol. Sci. 2023, 24(1), 376; https://doi.org/10.3390/ijms24010376 - 26 Dec 2022

Cited by 4 | Viewed by 1962

Abstract

The tumor microenvironment comprising blood vessels, fibroblasts, immune cells, and the extracellular matrix surrounding cancer cells, has recently been targeted for research in cancer therapy. We aimed to investigate the effect of macrophages on the invasive ability of gastric cancer cells, and studied their potential mechanism. In transcriptome analysis, integrin αV was identified as a gene increased in AGS cells cocultured with RAW264.7 cells. AGS cells cocultured with RAW264.7 cells displayed increased adhesion to the extracellular matrix and greater invasiveness compared with AGS cells cultured alone. This increased invasion of AGS cells cocultured with RAW264.7 cells was inhibited by integrin αV knockdown. In addition, the increase in integrin αV expression induced by tumor necrosis factor-α (TNF-α) or by coculture with RAW264.7 cells was inhibited by TNF receptor 1 (TNFR1) knockdown. The increase in integrin αV expression induced by TNF-α was inhibited by both Mitogen-activated protein kinase (MEK) inhibitor and VGLL1 S84 peptide treatment. Finally, transcription of integrin αV was shown to be regulated through the binding of VGLL1 and TEAD4 to the promoter of integrin αV. In conclusion, our study demonstrated that TNFR1–ERK–VGLL1 signaling activated by TNF-α secreted from RAW264.7 cells increased integrin αV expression, thereby increasing the adhesion and invasive ability of gastric cancer cells. Full article

(This article belongs to the Special Issue Future Challenges of Targeted Therapy of Cancers)

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