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Single-Cell Biology of Cancer
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Single-Cell Biology of Cancer

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

Deadline for manuscript submissions: 31 December 2026 | Viewed by 1351

Special Issue Editor

Dr. Chang Zou

E-Mail Website
Guest Editor
School of Medicine, Life and Health Sciences, The Chinese University of Hong Kong, Shenzhen 518172, China
Interests: precision medicine; drug resistance; heterogeneity of tumor microenvironment; multi-omics sequencing; epigenetic modifications; liquid biopsy

Special Issue Information

Dear Colleagues,

Single-cell biology is revolutionizing cancer research by decoding tumor heterogeneity at unprecedented resolution. It enables the identification of rare cell populations, such as cancer stem cells and therapy-resistant clones, that drive disease progression and relapse. By analyzing individual tumor, immune, and stromal cells, this approach maps the complex cellular ecosystems within malignancies. It reveals dynamic transcriptional states, evolutionary trajectories, and cell–cell communication networks that underlie treatment failure. This fine-grained understanding is pivotal for developing novel biomarkers and precision oncology strategies, moving beyond bulk tumor analysis to target the specific cellular drivers of cancer.

This Special Issue invites original research articles and reviews related to single-cell sequencing in cancer, including—but not limited to—the topics outlined above.

We look forward to receiving your contributions.

Dr. Chang Zou
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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

  • tumor heterogeneity
  • single-cell sequencing
  • drug resistance
  • tumor microenvironment
  • cell–cell communication
  • precision oncology

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Published Papers (2 papers)

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Research

25 pages, 7356 KB  
Article
Single-Cell and Spatial Transcriptomics Reveals Selenoproteins Shape Immunosuppressive Microenvironment and Therapeutic Outcomes in Glioma
by Xiaowei Zhang, Na Zhang, Yuqing Zhong, Siqi Ou, Guitao Wu, Taohui Ouyang and Kejun He
Cancers 2026, 18(9), 1489; https://doi.org/10.3390/cancers18091489 - 6 May 2026
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Abstract
Background: Gliomas exhibit substantial intratumoral heterogeneity, which limits prognostic precision and therapeutic efficacy. Selenoproteins are key regulators of redox homeostasis, but their role in glioma progression remains insufficiently defined. This study aimed to characterize glioma cells with high selenoprotein activity and to determine [...] Read more.
Background: Gliomas exhibit substantial intratumoral heterogeneity, which limits prognostic precision and therapeutic efficacy. Selenoproteins are key regulators of redox homeostasis, but their role in glioma progression remains insufficiently defined. This study aimed to characterize glioma cells with high selenoprotein activity and to determine their biological and clinical significance. Methods: We performed integrated multi-omic analyses combining bulk transcriptomic, single-cell transcriptomic, and spatial transcriptomic data to identify and characterize glioma cell states associated with elevated selenoprotein expression. Functional validation was conducted using SELENOS knockdown assays to evaluate effects on glioma proliferation, invasion, tumor growth, macrophage recruitment, CSF1 expression, and macrophage polarization. Results: We identified a malignant glioma cell state, termed SehighMali, characterized by elevated selenoprotein expression and distinct metabolic and immunological features. SehighMali cells showed enhanced oxidative phosphorylation, MYC-associated transcription, and DNA repair activity, and preferentially engaged in immunosuppressive crosstalk with myeloid cells through the CSF1–CSF1R axis. Spatial analyses demonstrated enrichment of SehighMali cells in tumor cores and close colocalization with immunosuppressive myeloid populations. Across bulk cohorts, higher SehighMali abundance was associated with aggressive molecular features, poor clinical outcomes, and a predicted temozolomide-resistant phenotype. SELENOS knockdown suppressed glioma proliferation, invasion, and tumor growth, reduced macrophage recruitment, decreased CSF1 expression, and promoted macrophage polarization toward a pro-inflammatory phenotype. Conclusions: These findings define a selenoprotein-driven malignant glioma state associated with immune evasion and therapeutic vulnerability. They further identify SELENOS as a potential therapeutic target and provide insight into how selenoprotein-related programs contribute to glioma progression. Full article
(This article belongs to the Special Issue Single-Cell Biology of Cancer)
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16 pages, 3902 KB  
Article
Single-Cell Dissection Identifies METTL7B as Associated with Cell Adhesion-Mediated Tumor Invasion in Lung Adenocarcinoma and Glioblastoma
by Jie Mao, Jinquan Xia, Huibin Song, Fuhua Zhong, Huiyi Feng, Junhui Chen and Guangsuo Wang
Cancers 2026, 18(9), 1384; https://doi.org/10.3390/cancers18091384 - 27 Apr 2026
Viewed by 461
Abstract
Background: Tumor invasion is the central barrier to effective immunotherapy in lung adenocarcinoma (LUAD) and glioblastoma. Cell adhesion signaling critically shapes tumor–microenvironment interactions, yet the upstream regulators coordinating these invasive programs at single-cell resolution remain incompletely understood. Methyltransferase Like protein 7B (METTL7B) [...] Read more.
Background: Tumor invasion is the central barrier to effective immunotherapy in lung adenocarcinoma (LUAD) and glioblastoma. Cell adhesion signaling critically shapes tumor–microenvironment interactions, yet the upstream regulators coordinating these invasive programs at single-cell resolution remain incompletely understood. Methyltransferase Like protein 7B (METTL7B) has recently emerged as a candidate oncogenic regulator, but its lineage-specific functions and the potential downstream effectors are unclear. Methods: We integrated publicly available single-cell RNA sequencing datasets from LUAD and glioblastoma with The Cancer Genome Atlas (TCGA) transcriptomic analyses to resolve METTL7B-associated malignant cell states and microenvironmental interactions. Functional enrichment analyses identified invasion- and focal adhesion pathways linked to METTL7B expression. Gain- and loss-of-function experiments were conducted in LUAD and glioblastoma cell lines to validate downstream cell adhesion effectors. Spatial expression patterns were examined using immunofluorescence, and transwell assays were used to assess migratory and invasive phenotypes. Results: Single-cell analyses revealed that METTL7B was selectively enriched in malignant epithelial cells in LUAD and glioblastoma and defined a transcriptional program characterized by cell adhesion signaling. Integrin Alpha 3 (ITGA3) emerged as a conserved downstream effector of METTL7B, with progressive upregulation from minimally invasive to invasive LUAD and glioblastoma. Functional perturbation confirmed that METTL7B enhances tumor cell migration and invasion through integrin-associated pathways. Conclusions: METTL7B acts as a potential lineage-enriched regulator of invasive tumor states by activating cell adhesion signaling in LUAD and glioblastoma. These findings position METTL7B as a putative prognostic factor for strategies aimed at limiting invasion in lung cancer and glioblastoma. Full article
(This article belongs to the Special Issue Single-Cell Biology of Cancer)
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