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The Cellular Ecosystem of Cancer: New Insights into Cell Biology

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 2640

Special Issue Editors


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Guest Editor
Department of Medicine, Tulane University School of Medicine, Louisiana Cancer Research Center, New Orleans, LA, USA
Interests: lung cancer; metastasis; EMT; Golgi apparatus; secretion; intracellular trafficking

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Guest Editor
Department of Toxicology and Cancer Biology, The University of Kentucky, Lexington, KY, USA
Interests: membrane trafficking; microscopy; EMT; lung adenocarcinoma

Special Issue Information

Dear Colleagues,

Dysregulation of key cellular organelles—including the endoplasmic reticulum (ER), mitochondria, lysosomes, Golgi apparatus, and others—has emerged as a critical factor in cancer progression. Cancer cells actively remodel these organelles to sustain rapid proliferation and to reshape the tumor microenvironment.

Despite their fundamental importance, therapies directly targeting organelle function have achieved limited success. One major challenge lies in the fact that these organelles are also essential for normal cell survival. Therefore, an effective strategy requires identifying cancer-specific vulnerabilities—such as genetic alterations or hyperactivated pathways—that are indispensable for tumor cells but dispensable for normal tissues.

A deeper understanding of how cancer cells remodel organelle structure and function, and the key regulators involved in this process, will open new avenues for therapeutic intervention. This Special Issue will highlight recent advances in uncovering the diverse roles of cellular organelles in cancer biology and their potential as novel therapeutic targets.

Dr. Xiaochao Tan
Dr. Guan-Yu Xiao
Guest Editors

Manuscript Submission Information

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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

  • cell organelle
  • ER
  • mitochondria
  • lysosome
  • Golgi
  • secretion
  • tumor microenvironment

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Published Papers (2 papers)

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Review

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15 pages, 1016 KB  
Review
Rewiring Dendritic Cell Immunity: The β-Catenin–TIM-3 Axis as a Target to Improve DC Cancer Vaccines
by Chunmei Fu, Tianle Ma, Li Zhou, Qing-Sheng Mi and Aimin Jiang
Cancers 2026, 18(2), 201; https://doi.org/10.3390/cancers18020201 - 8 Jan 2026
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Abstract
The success of cancer vaccines relies on the ability of dendritic cells (DCs) to efficiently prime cytotoxic CD8 T cell responses against tumors. However, in solid tumors this process is often undermined by tumor-driven immunosuppression and intrinsic defects in DC activation. Among the [...] Read more.
The success of cancer vaccines relies on the ability of dendritic cells (DCs) to efficiently prime cytotoxic CD8 T cell responses against tumors. However, in solid tumors this process is often undermined by tumor-driven immunosuppression and intrinsic defects in DC activation. Among the signaling pathways implicated in DC dysfunction, β-catenin signaling has emerged as a key regulator of immune tolerance in DCs. In parallel, inhibitory receptors such as PD-L1 and TIM-3 on DCs have been recognized as critical DC-intrinsic brakes on CD8 T cell priming and on responses to immune checkpoint blockade (ICB). Recent work has identified a DC-intrinsic immunoregulatory circuit in which β-catenin activation in DCs—particularly in cross-presenting cDC1s—induces expression of TIM-3, thereby suppressing CD8 T cell cross-priming and limiting anti-tumor CD8 T cell immunity. This β-catenin–TIM-3 axis represents a previously underappreciated layer of negative regulation that may help explain, at least in part, the limited efficacy of many current DC-based cancer vaccines. In this review, we examine how β-catenin activation in DCs, particularly in cDC1s, induces TIM-3 and related inhibitory programs that suppress cross-priming of tumor antigen-specific CD8 T cells and constrain the efficacy of DC-based vaccines. We further discuss how selectively targeting this β-catenin–TIM-3 checkpoint axis—alone or together with PD-L1 and other β-catenin–linked receptors—could restore DC function and inform rational combinations of DC-based vaccination with ICB and other T cell-based immunotherapies. Full article
(This article belongs to the Special Issue The Cellular Ecosystem of Cancer: New Insights into Cell Biology)
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10 pages, 688 KB  
Commentary
QSOX1: A Mysterious Golgi-Localized Disulfide Bond Catalyst and an Emerging Cancer Regulator
by Shike Wang, Guan-Yu Xiao and Xiaochao Tan
Cancers 2026, 18(2), 339; https://doi.org/10.3390/cancers18020339 - 21 Jan 2026
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Abstract
Quiescin sulfhydryl oxidase 1 (QSOX1) is a disulfide bond-forming enzyme with both disulfide isomerase and oxidoreductase activities. It plays an important role in protein folding, stability, and secretion. Growing evidence demonstrates that QSOX1 is upregulated in multiple cancer types and influences key behaviors [...] Read more.
Quiescin sulfhydryl oxidase 1 (QSOX1) is a disulfide bond-forming enzyme with both disulfide isomerase and oxidoreductase activities. It plays an important role in protein folding, stability, and secretion. Growing evidence demonstrates that QSOX1 is upregulated in multiple cancer types and influences key behaviors of cancer cells, including proliferation, migration, invasion, and metastasis. Elevated QSOX1 expression is also associated with tumor malignancy and disease relapse. However, the molecular mechanisms by which QSOX1 drives cancer progression remain incompletely understood. In this review, we summarize current knowledge of QSOX1 expression and regulation in cancer, discuss its functional roles, and highlight key unanswered questions to warrant further investigation. Full article
(This article belongs to the Special Issue The Cellular Ecosystem of Cancer: New Insights into Cell Biology)
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