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Signaling Pathways Dysregulation in Cancer: Advances and New Therapeutics Hopes
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Signaling Pathways Dysregulation in Cancer: Advances and New Therapeutics Hopes

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: 20 January 2025 | Viewed by 6539

Special Issue Editor

Dr. Daniela Miricescu

E-Mail Website
Guest Editor
Department of Biochemistry, Faculty of Dentistry, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania
Interests: PI3K/AKT/mTOR; oxidative stress; breast cancer; burns; colorectal cancer; PLGA nanoparticles; platelet rich plasma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Malignant neoplasms, characterized by successive genetic and epigenetic alterations of healthy cells, are one of the leading causes of death within the adult population. Usually, most cancers emerge at the epithelial cells, leading to organ-specific carcinomas affecting skin, liver, lung, breast, or pancreas. Since oncogenic mutations induce gene overexpression and subsequently cause protein dysregulation, the PI3K/AKT/mTOR, TGF-β family, Ras/Raf/MEK/ERK, and the Wnt/β-catenin signaling pathway dysregulations are correlated with the proliferation, angiogenesis, invasion, and metastasis of cancer cells. Therefore, inhibitors targeting these pathways are considered as novel therapeutic candidates for the development of potential anticancer agents.

We cordially invite submissions of original research and comprehensive review articles for inclusion in this Special Issue.

This Special Issue is overseen by Dr. Daniela Miricescu with the assistance of Dr. Constantin Stefani ( Department of Family Medicine and Clinical Base, Dr. Carol Davila Central Military Emergency University Hospital).

Dr. Daniela Miricescu
Guest Editor

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Keywords

  • cancer
  • epithelial cells
  • oncogenic mutations
  • PI3K/AKT/mTOR
  • TGF-β
  • Ras/Raf/MEK/ERK
  • Wnt/β-catenin
  • angiogenesis
  • invasion
  • metastasis
  • inhibitors

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Published Papers (2 papers)

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Research

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15 pages, 3305 KiB  
Article
SPRED2 Is a Novel Regulator of Autophagy in Hepatocellular Carcinoma Cells and Normal Hepatocytes
by Tianyi Wang, Tong Gao, Masayoshi Fujisawa, Toshiaki Ohara, Masakiyo Sakaguchi, Teizo Yoshimura and Akihiro Matsukawa
Int. J. Mol. Sci. 2024, 25(11), 6269; https://doi.org/10.3390/ijms25116269 - 6 Jun 2024
Cited by 1 | Viewed by 1316
Abstract
Sprouty-related enabled/vasodilator-stimulated phosphoprotein homology 1 domain containing 2 (SPRED2) is an inhibitor of the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway and has been shown to promote autophagy in several cancers. Here, we aimed to determine whether SPRED2 plays a role in [...] Read more.
Sprouty-related enabled/vasodilator-stimulated phosphoprotein homology 1 domain containing 2 (SPRED2) is an inhibitor of the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway and has been shown to promote autophagy in several cancers. Here, we aimed to determine whether SPRED2 plays a role in autophagy in hepatocellular carcinoma (HCC) cells. The Cancer Genome Atlas (TCGA) Liver Cancer Database showed a negative association between the level of SPRED2 and p62, a ubiquitin-binding scaffold protein that accumulates when autophagy is inhibited. Immunohistochemically, accumulation of p62 was detected in human HCC tissues with low SPRED2 expression. Overexpression of SPRED2 in HCC cells increased the number of autophagosomes and autophagic vacuoles containing damaged mitochondria, decreased p62 levels, and increased levels of light-chain-3 (LC3)-II, an autophagy marker. In contrast, SPRED2 deficiency increased p62 levels and decreased LC3-II levels. SPRED2 expression levels were negatively correlated with translocase of outer mitochondrial membrane 20 (TOM20) expression levels, suggesting its role in mitophagy. Mechanistically, SPRED2 overexpression reduced ERK activation followed by the mechanistic or mammalian target of rapamycin complex 1 (mTORC1)-mediated signaling pathway, and SPRED2 deficiency showed the opposite pattern. Finally, hepatic autophagy was impaired in the liver of SPRED2-deficient mice with hepatic lipid droplet accumulation in response to starvation. These results indicate that SPRED2 is a critical regulator of autophagy not only in HCC cells, but also in hepatocytes, and thus the manipulation of this process may provide new insights into liver pathology. Full article
(This article belongs to the Special Issue Signaling Pathways Dysregulation in Cancer: Advances and New Therapeutics Hopes)
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Review

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26 pages, 1785 KiB  
Review
Targeting PI3K/AKT/mTOR and MAPK Signaling Pathways in Gastric Cancer
by Diana-Theodora Morgos, Constantin Stefani, Daniela Miricescu, Maria Greabu, Silviu Stanciu, Silvia Nica, Iulia-Ioana Stanescu-Spinu, Daniela Gabriela Balan, Andra-Elena Balcangiu-Stroescu, Elena-Claudia Coculescu, Dragos-Eugen Georgescu and Remus Iulian Nica
Int. J. Mol. Sci. 2024, 25(3), 1848; https://doi.org/10.3390/ijms25031848 - 3 Feb 2024
Cited by 18 | Viewed by 4603
Abstract
Gastric cancer (GC) is the fourth leading cause of death worldwide, with more than 1 million cases diagnosed every year. Helicobacter pylori represents the main risk factor, being responsible for 78% of the cases. Increased amounts of salt, pickled food, red meat, alcohol, [...] Read more.
Gastric cancer (GC) is the fourth leading cause of death worldwide, with more than 1 million cases diagnosed every year. Helicobacter pylori represents the main risk factor, being responsible for 78% of the cases. Increased amounts of salt, pickled food, red meat, alcohol, smoked food, and refined sugars negatively affect the stomach wall, contributing to GC development. Several gene mutations, including PIK3CA, TP53, ARID1A, CDH1, Ras, Raf, and ERBB3 are encountered in GC pathogenesis, leading to phosphatidylinositol 3-kinase (PI3K) protein kinase B (AKT)/mammalian target of rapamycin (mTOR)—PI3K/AKT/mTOR—and mitogen-activated protein kinase (MAPK) signaling pathway activation and promoting tumoral activity. Helicobacter pylori, growth factors, cytokines, hormones, and oxidative stress also activate both pathways, enhancing GC development. In clinical trials, promising results have come from monoclonal antibodies such as trastuzumab and ramucirumab. Dual inhibitors targeting the PI3K/AKT/mTOR and MAPK signaling pathways were used in vitro studies, also with promising results. The main aim of this review is to present GC incidence and risk factors and the dysregulations of the two protein kinase complexes together with their specific inhibitors. Full article
(This article belongs to the Special Issue Signaling Pathways Dysregulation in Cancer: Advances and New Therapeutics Hopes)
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