International Journal of Molecular Sciences

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Dear Colleagues,

This Special Issue, “Signal Pathways Involved in Resistance to Apoptosis in Cancer”, will cover a selection of recent research topics and current review articles related to the intracellular signaling of resistance to apoptosis in cancer. Up-to-date review articles, commentaries, and experimental papers are all welcome.

Programmed cell death or apoptosis is a natural mechanism by which organisms control the number of cells. It plays an important role in embryonic development and maintaining cell homeostasis. The deregulation of apoptosis machinery induces resistance to apoptosis. This resistance is characterized by the inhibition of cell death triggering or delay in cell death unfolding in response to an apoptotic stimulus. Apoptosis resistance plays an important role in tumor development. Uncontrolled cell proliferation combined with resistance to apoptosis is both necessary and sufficient for tumor progression to a malignant phenotype. Although there are several mechanisms by which cells escape apoptosis, the majority of these lead to an inability of the cell to trigger the intrinsic pathway of apoptosis (called the mitochondrial pathway). Despite numerous studies of the pathways in the apoptosis resistance mechanism, the involved signaling pathways have not yet been fully elucidated, and there are disparities regarding their role in this mechanism.

Prof. Dr. Bertrand Liagre
Guest Editor

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Keywords

cancer
signal pathway
apoptosis
targeted therapy

Published Papers (1 paper)

Research

22 pages, 9840 KiB

Open AccessArticle

Cathepsin H Knockdown Reverses Radioresistance of Hepatocellular Carcinoma via Metabolic Switch Followed by Apoptosis

by Qiao Chen, Shugen Qu, Zhenzhen Liang, Yi Liu, Huajian Chen, Shumei Ma and Xiaodong Liu

Int. J. Mol. Sci. 2023, 24(6), 5257; https://doi.org/10.3390/ijms24065257 - 9 Mar 2023

Cited by 1 | Viewed by 1631

Abstract

Despite the wide application of radiotherapy in HCC, radiotherapy efficacy is sometimes limited due to radioresistance. Although radioresistance is reported with high glycolysis, the underlying mechanism between radioresistance and cancer metabolism, as well as the role of cathepsin H (CTSH) within it, remain unclear. In this study, tumor-bearing models and HCC cell lines were used to observe the effect of CTSH on radioresistance. Proteome mass spectrometry, followed by enrichment analysis, were used to investigate the cascades and targets regulated by CTSH. Technologies such as immunofluorescence co-localization flow cytometry and Western blot were used for further detection and verification. Through these methods, we originally found CTSH knockdown (KD) perturbed aerobic glycolysis and enhanced aerobic respiration, and thus promoted apoptosis through up-regulation and the release of proapoptotic factors such as AIFM1, HTRA2, and DIABLO, consequently reducing radioresistance. We also found that CTSH, together with its regulatory targets (such as PFKL, HK2, LDH, and AIFM1), was correlated with tumorigenesis and poor prognosis. In summary, our study found that the cancer metabolic switch and apoptosis were regulated by CTSH signaling, leading to the occurrence of radioresistance in HCC cells and suggesting the potential value of HCC diagnosis and therapy. Full article

(This article belongs to the Special Issue Signal Pathways Involved in Resistance to Apoptosis in Cancer)

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