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Cancers
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Molecular Landscape in Liver, Pancreas and Gastrointestinal Tumors
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Molecular Landscape in Liver, Pancreas and Gastrointestinal Tumors

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 6243

Special Issue Editor

Dr. Francesco Vasuri

E-Mail Website
Guest Editor
Pathology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Via Albertoni 15, 40138 Bologna, Italy
Interests: histopathology; GI and liver pathology; molecular biology; neoangiogenesis; transplant pathology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Molecular biology has become a fundamental component of histopathology labs for the routine practice of most patients with malignant tumors, for diagnosis, prognostic stratification, and the identification of markers for targeted therapies. Among the gastrointestinal cancers, there is a disequilibrium between some cancers that are relatively well studied from a molecular point of view (e.g., colorectal adenocarcinoma) and other cancers (e.g., hepatocellular and cholangiocellular carcinoma) in which the molecular landscape is much less investigated.

This Special Issue focuses on the study of the diagnostic, prognostic and predictive molecular markers in liver, pancreas and gastrointestinal tumors. The Special Issue, launched by Cancers, is dedicated to answering diagnostic and biological unsolved questions in GI cancers. Researchers are also encouraged to submit original research on new insights for known and well-established markers in the pathological mechanisms and molecular pathways of neoplasms of the GI tract, pancreas, liver and biliary tract. Review articles describing the state of the art and systematic reviews on this topic are also encouraged. The main areas of interest are:

  • GI tract tumors.
  • Pancreatic tumors.
  • Liver tumors.
  • Biliary tract tumors.

Dr. Francesco Vasuri
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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • GI tumors
  • liver tumors
  • molecular biology
  • pancreas tumors
  • molecular markers

Published Papers (3 papers)

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Research

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20 pages, 8117 KiB  
Article
Circular RNA CDR1as Mediated by Human Antigen R (HuR) Promotes Gastric Cancer Growth via miR-299-3p/TGIF1 Axis
by Rong Li, Xuejing Xu, Shuo Gao, Junyi Wang, Jie Hou, Zhenfan Xie, Lan Luo, Han Shen, Wenrong Xu and Jiajia Jiang
Cancers 2023, 15(23), 5556; https://doi.org/10.3390/cancers15235556 - 23 Nov 2023
Cited by 1 | Viewed by 1220
Abstract
Background: Gastric cancer (GC) remains a common malignancy worldwide with a limited understanding of the disease mechanisms. A novel circular RNA CDR1as has been recently reported to be a crucial regulator of human cancer. However, its biological role and mechanism in the GC [...] Read more.
Background: Gastric cancer (GC) remains a common malignancy worldwide with a limited understanding of the disease mechanisms. A novel circular RNA CDR1as has been recently reported to be a crucial regulator of human cancer. However, its biological role and mechanism in the GC growth are still far from clear. Methods: Small interfering RNAs (siRNAs), lentivirus or plasmid vectors were applied for gene manipulation. The CDR1as effects on the GC growth were evaluated in CCK8 and colony formation assays, a flow cytometry analysis and mouse xenograft tumor models. A bioinformatics analysis combined with RNA immunoprecipitation (RIP), RNA pull-down assays, dual-luciferase reporter gene assays, Western blot, reverse transcription–quantitative polymerase chain reaction (RT-qPCR) and functional rescue experiments were used to identify the CDR1as target miRNA, the downstream target gene and its interaction with human antigen R (HuR). Results: The CDR1as overexpression promoted the GC growth in vitro and in vivo and reduced the apoptotic rate of GC cells. Its knockdown inhibited the GC cell proliferation and viability and increased the cell apoptotic rate. Proliferation-related proteins PCNA and Cyclin D1 and apoptosis-related proteins Bax, Bcl-2, Caspase-3 and Caspase-9 were regulated. Mechanically, the cytoplasmic CDR1as acted as a miR-299-3p sponge to relieve its suppressive effects on the GC cell growth. Oncogenic TGIF1 was a miR-299-3p downstream target gene that mediated the promotive effects of CDR1as and regulated the PCNA and Bax levels. HuR interacted with CDR1as via the RRM2 domain and positively regulated the CDR1as level and its oncogenic role as well as downstream target TGIF1. Conclusions: CDR1as promotes the GC growth through the HuR/CDR1as/miR-299-3p/TGIF1 axis and could be used as a new therapeutic target for GC. Full article
(This article belongs to the Special Issue Molecular Landscape in Liver, Pancreas and Gastrointestinal Tumors)
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23 pages, 43660 KiB  
Article
CPSF3 Promotes Pre-mRNA Splicing and Prevents CircRNA Cyclization in Hepatocellular Carcinoma
by Ying Huang, Haofei Ji, Jiani Dong, Xueying Wang, Zhilin He, Zeneng Cheng and Qubo Zhu
Cancers 2023, 15(16), 4057; https://doi.org/10.3390/cancers15164057 - 11 Aug 2023
Viewed by 1170
Abstract
CircRNAs are crucial in tumorigenesis and metastasis, and are comprehensively downregulated in hepatocellular carcinoma (HCC). Previous studies demonstrated that the back-splicing of circRNAs was closely related to 3′-end splicing. As a core executor of 3′-end cleavage, we hypothesized that CPSF3 modulated circRNA circularization. [...] Read more.
CircRNAs are crucial in tumorigenesis and metastasis, and are comprehensively downregulated in hepatocellular carcinoma (HCC). Previous studies demonstrated that the back-splicing of circRNAs was closely related to 3′-end splicing. As a core executor of 3′-end cleavage, we hypothesized that CPSF3 modulated circRNA circularization. Clinical data were analyzed to establish the prognostic correlations. Cytological experiments were performed to determine the role of CPSF3 in HCC. A fluorescent reporter was employed to explore the back-splicing mechanism. The circRNAs regulated by CPSF3 were screened by RNA-seq and validated by PCR, and changes in downstream pathways were explored by molecular experiments. Finally, the safety and efficacy of the CPSF3 inhibitor JTE-607 were verified both in vitro and in vivo. The results showed that CPSF3 was highly expressed in HCC cells, promoting their proliferation and migration, and that a high CPSF3 level was predictive of a poor prognosis. A mechanistic study revealed that CPSF3 enhanced RNA cleavage, thereby reducing circRNAs, and increasing linear mRNAs. Furthermore, inhibition of CPSF3 by JET-607 suppressed the proliferation of HCC cells. Our findings indicate that the increase of CPSF3 in HCC promotes the shift of pre-mRNA from circRNA to linear mRNA, leading to uncontrolled cell proliferation. JTE-607 exerted a therapeutic effect on HCC by blocking CPSF3. Full article
(This article belongs to the Special Issue Molecular Landscape in Liver, Pancreas and Gastrointestinal Tumors)
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Review

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23 pages, 2492 KiB  
Review
MASLD and the Development of HCC: Pathogenesis and Therapeutic Challenges
by Anju G. S. Phoolchund and Salim I. Khakoo
Cancers 2024, 16(2), 259; https://doi.org/10.3390/cancers16020259 - 6 Jan 2024
Cited by 5 | Viewed by 3493
Abstract
Metabolic-dysfunction-associated steatotic liver disease (MASLD, previously known as non-alcoholic fatty liver disease (NAFLD)) represents a rapidly increasing cause of chronic liver disease and hepatocellular carcinoma (HCC), mirroring increasing rates of obesity and metabolic syndrome in the Western world. MASLD-HCC can develop at an [...] Read more.
Metabolic-dysfunction-associated steatotic liver disease (MASLD, previously known as non-alcoholic fatty liver disease (NAFLD)) represents a rapidly increasing cause of chronic liver disease and hepatocellular carcinoma (HCC), mirroring increasing rates of obesity and metabolic syndrome in the Western world. MASLD-HCC can develop at an earlier stage of fibrosis compared to other causes of chronic liver disease, presenting challenges in how to risk-stratify patients to set up effective screening programmes. Therapeutic decision making for MASLD-HCC is also complicated by medical comorbidities and disease presentation at a later stage. The response to treatment, particularly immune checkpoint inhibitors, may vary by the aetiology of the disease, and, in the future, patient stratification will be key to optimizing the therapeutic pathways. Full article
(This article belongs to the Special Issue Molecular Landscape in Liver, Pancreas and Gastrointestinal Tumors)
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