Multiple Roles of the RB Family of Tumor Suppressors and Implications for Cancer Therapy

Dear Colleagues,

The RB1 protein—the first tumor suppressor—was discovered in the 1980s and, since then, its pathway has been found to be inactivated in most cancers. According to the canonical model, the tumor-suppressive activity of RB1 depends on its ability to restrain cell proliferation. However, evidence has shown RB1’s mode of action to be much more complex, with this factor undergoing different post-translational modifications and multiple protein interactions, whereby it controls a multitude of functions. These functions include DNA repair, preservation of chromosomal stability, cell death, senescence, immune response, metabolism, epithelial–mesenchymal transition, angiogenesis, stemness, cell lineage identity, and differentiation, the deregulation of which underlies both cancer onset and progression and impacts on the response to anticancer treatments. Thus, RB1 has emerged as an appealing therapeutic target and candidate to support therapeutic decisions.

However, the complexity of RB1’s functions, which remain controversial and underexplored in various contexts, and the difficulties in evaluating RB1’s functional status hinder the clinical translation of approaches aimed at exploiting the predictive, prognostic, and therapeutic value of this tumor suppressor. Moreover, RB1 belongs to a family of proteins, including RBL1/p107 and RBL2/p130, that have both overlapping and distinct functions. Although the key role of these other two RB family members (especially that of RBL2/p130) in cell-cycle exit events is well-recognized, there are much less data on the mechanisms of action of these proteins. This Special Issue will cover all of the aspects of the biology of RB proteins, with a particular focus on their emerging non-canonical functions and their involvement in the response to conventional treatments, targeted therapies, and immunotherapeutic approaches. Moreover, possible strategies exploiting RB family members therapeutically will be discussed. We hope that this Special Issue will help us to better understand the role of these crucial proteins in the neoplastic process and in cancer therapy and will point to new directions to tackle clinical translational hurdles. 

Dr. Paola Indovina
Dr. Francesca Pentimalli
Prof. Antonio Giordano
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 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-anonymized 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.