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Cells
Special Issues
How Does Gene Regulation Affect Cancer Development?
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How Does Gene Regulation Affect Cancer Development?

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 1482

Special Issue Editors

Prof. Dr. Ru Chih C. Huang

E-Mail Website
Guest Editor
1. Department of Biology, Zanvyl Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD 21218-2685, USA
2. National Academy of Inventors, Tampa, FL 33612, USA
3. Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei 11529, Taiwan
Interests: chromatin structure and function; tetra-O-methyl nordihydroguaiaretic acid (M4N, terameprocol); oncogenic development in humans; chemotherapeutic drug treatments; viral replication; gene functions
Special Issues, Collections and Topics in MDPI journals
Dr. Kotohiko Kimura

E-Mail Website
Guest Editor
Department of Biology, Johns Hopkins University, 3400 N. Charles Street, Baltimore, MD 21218-2685, USA
Interests: anticancer drug; combination drug treatment; transcription factor; gene regulation; alternative splicing; cancer metabolism; mitochondria; apoptosis and hypoxia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The mutations of certain genes greatly contribute to oncogenesis and cancer development. Some mutations occur in the open reading frame of genes, while other mutations occur in the regulatory domains of genes. The former type of mutations are cancer-specific and, therefore, difficult to target using anticancer drug developments. Meanwhile, the latter types of mutations lead to either the upregulation or downregulation of certain genes and, therefore, might provide some way to control the expression of these genes by manipulating some cellular regulatory mechanisms, such as transcription factors, non-coding RNAs, histones, and others. We recently proposed that the suppression of SP1, MYC, and HIF1A altogether could be a good target for anticancer drug development because cancers often use these transcription factors to their advantage. This Special Issue aims to further examine cellular gene networks that are utilized by cancers for their development, and which could be potential targets of anticancer drug development.

Prof. Dr. Ru Chih C. Huang
Dr. Kotohiko Kimura
Guest Editors

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 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. Cells 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 2700 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

  • cancer
  • mutation
  • transcription factor
  • non-coding RNA
  • micro-RNA
  • gene regulation
  • histones
  • gene promoters
  • anticancer drugs

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Published Papers (1 paper)

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Research

14 pages, 36585 KB  
Article
Integrated Multi-Omics and Spatial Transcriptomics Identify FBLL1 as a Malignant Transformation Driver in Hepatocellular Carcinoma
by Junye Xie, Shujun Guo, Yujie Xiao, Yibo Zhang, An Hong and Xiaojia Chen
Cells 2026, 15(3), 246; https://doi.org/10.3390/cells15030246 - 27 Jan 2026
Viewed by 971
Abstract
Background: Hepatocellular carcinoma (HCC) is characterized by marked intratumoral heterogeneity and poor clinical outcomes. Dysregulated ribosome biogenesis has emerged as a fundamental hallmark of tumor initiation and progression; however, the specific molecular drivers linking this machinery to HCC pathogenesis remain largely undefined. [...] Read more.
Background: Hepatocellular carcinoma (HCC) is characterized by marked intratumoral heterogeneity and poor clinical outcomes. Dysregulated ribosome biogenesis has emerged as a fundamental hallmark of tumor initiation and progression; however, the specific molecular drivers linking this machinery to HCC pathogenesis remain largely undefined. Methods: By integrating multi-omics data from the TCGA and ICGC cohorts, FBLL1 was identified as a key prognostic candidate gene. Its cellular and spatial distribution was analyzed using single-cell RNA sequencing and spatial transcriptomics. Its biological functions in vitro and in vivo were validated through functional experiments, including lentivirus-mediated ectopic expression and siRNA-mediated gene knockdown. Finally, its molecular mechanism was elucidated through transcriptomic analysis and Western blotting. Results: FBLL1 was significantly upregulated in HCC and correlated with poor patient survival. Spatial and single-cell analyses showed that FBLL1 expression was preferentially enriched in malignant hepatocytes within the tumor region. Functionally, knockdown FBLL1 could inhibit the proliferation and clonogenic capacity of HCC cells, while overexpression FBLL1 in non-tumorigenic hepatocytes could promote the tumorigenic phenotype in xenograft models. Transcriptomic analysis indicated that FBLL1 overexpression was associated with the synergistic upregulation of c-Myc and multiple EGFR ligands, as well as decreased expression of hepatocyte functional markers. Consistently, modulation of FBLL1 expression affected the activity of the EGFR–MAPK signaling pathway. Conclusions: Our study identifies FBLL1 as a previously unrecognized regulator associated with malignant state transition in HCC. Rather than acting as a direct regulator of core signaling components, FBLL1 is associated with ligand-dependent activation of the EGFR–MAPK pathway in conjunction with c-Myc upregulation. These findings indicate that FBLL1 represents a promising therapeutic target for disrupting oncogenic signaling programs in liver cancer. Full article
(This article belongs to the Special Issue How Does Gene Regulation Affect Cancer Development?)
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