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Cancer Related Molecular Mechanisms Research · Journal article
Medical Sciences · August 10, 2026
Raises a question worth testing. It does not answer one.
This narrative review synthesizes literature on autophagy's dual role in cancer progression and its regulation by miRNAs, proposing that combination therapies targeting autophagy inhibition plus standard agents may overcome treatment resistance in advanced prostate cancer. The conclusions are based on mechanistic understanding and preclinical potential rather than clinical trial data, and represent conceptual framework and hypotheses for future testing.
Narrative literature review. Advanced prostate cancer; general oncology.
Autophagy acts as a 'double-edged sword', functioning both as cellular protective shield against metabolic stress and as potential pathway to autophagic cell death Specific miRNA molecules (miR-21, miR-141, miR-375) regulate autophagic machinery and serve as potential circulating biomarkers Autophagy regulation involves crosstalk with apoptotic pathways mediated by Bcl-2 family proteins, kinases (mTOR, JNK, DAPK), and p53
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This review identifies autophagy modulation via miRNA as a conceptual translational target and proposes specific combination strategies (autophagy inhibitors plus standard therapy) as a hypothesis for overcoming treatment resistance. However, no clinical efficacy data are presented; the conclusions rest on mechanistic rationale and preclinical work requiring clinical validation.
This is a narrative literature review proposing mechanistic hypotheses about autophagy, miRNA regulation, and combination therapy in prostate cancer, without reporting original experimental or clinical data.
As stated by the source record.
This review identifies autophagy modulation via miRNA as a conceptual translational target and proposes specific combination strategies (autophagy inhibitors plus standard therapy) as a hypothesis for overcoming treatment resistance. However, no clinical efficacy data are presented; the conclusions rest on mechanistic rationale and preclinical work requiring clinical validation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Background: Autophagy is a process that diversely impacts the stages of both tumor initiation and progression. Elucidating the molecular mechanisms underlying autophagy and its role in tumorigenesis is a key component of anticancer strategies in both prostate cancer and other malignancies. Because advanced prostate cancer frequently exploits enhanced autophagy as a defense mechanism against therapy-induced stress (e.g., from abiraterone), the pharmacological modulation of miRNA levels presents a tremendous opportunity to block the tumor’s escape route and overcome drug resistance. Methods: A comprehensive literature review was conducted to evaluate the molecular pathways determining cancer cell survival and death. The analysis focused on the dual nature of autophagy (functioning as a ‘double-edged sword’) within the tumor microenvironment, microRNA (miRNA) regulatory networks, and the efficacy of synergistic therapeutic strategies in overcoming treatment resistance. Results: The primary focus of this paper is the dual and complex role of autophagy, which serves, on the one hand, as a cellular protective shield against metabolic stress—thereby facilitating metastasis—and, on the other hand, as a potential pathway leading to autophagic cell death. The progression of this crucial process is regulated by intricate interactions (crosstalk) with apoptotic pathways, mediated by Bcl-2 family proteins, key kinases (such as mTOR, JNK, and DAPK), and transcription factors, such as p53. Furthermore, the autophagic machinery is precisely regulated by specific miRNA molecules (e.g., miR-21, miR-141, and miR-375). These not only act as crucial intracellular modulators of autophagy but also serve as promising circulating biomarkers, enabling the monitoring of this process’s activity throughout disease progression. Conclusions: Autophagy, and in particular its modulation via miRNA signaling networks, represents a major and highly promising translational target. By directly impairing this autophagic survival mechanism, ‘double-hit’ combination therapies—integrating autophagy inhibitors (such as hydroxychloroquine or VPS34 inhibitors) with standard antiandrogen or cytotoxic agents—demonstrate promising preclinical potential in overcoming treatment resistance and favorably modulating the immune microenvironment in advanced prostate cancer.
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