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Updated: Aug 5, 2026

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Published on: September 10, 2018
Nanomedicine-Mediated Autophagy Modulation in Placental Impairment Versus Cancers: A Narrative Review
Melinda Ildiko Mitranovici1,2, Viviana Ivan3, Adrian Apostol3
1Department of Obstetrics and Gynecology, Emergency County Hospital Hunedoara, 331057 Hunedoara, Romania.
Abstract:
The biggest challenge faced by classical anticancer therapy is drug resistance, which causes cancer recurrence and metastasis. Two underlying mechanisms could be responsible, including the stemness of pro-survival autophagy-associated cancer stem cells (CSCs). Background/Objectives: The relationship between CSCs and autophagy in gynecological cancer is still unknown. However, it has been shown that CSCs' in vitro self-renewal ability is decreased when autophagy is inhibited. Helping to maintain normal tissue homeostasis, autophagy is a catabolic process involved in degrading long-lived proteins and cytoplasmic organelles. Autophagy acts as a key player in the human body's self-regenerating tissues. It also has a reproductive function, contributing to decidualization for a successful pregnancy. The aim of our review is to identify similarities and differences between these processes, using these findings to discover new therapeutic strategies through nanotechnology. Method: We conducted a narrative review, identifying heterogeneity in the data in the literature, and found 153 relevant articles. Discussions: While autophagy has been proven to be capable of acting as a tumor suppressor, it also promotes tumor progression. Moreover, it has been linked to cancer stem cell regulation, therapy resistance, cancer invasion, and metastasis. Several molecular mechanisms have been linked to autophagy. Remarkably, some cellular processes required for proper placentation, including autophagy, are common between placental development and tumor growth. Just as trophoblast cells invade and migrate, so do cancer cells. While in the trophoblast, this phenomenon is programmed and controlled; in cancer, this regulation is lost. As shown, we thus observed commonalities and discrepancies in the phenotypes and underlying molecular mechanisms of autophagy regulation in preeclampsia versus cancer contexts. Translational applicability of nanomedicine research strategies and design paradigms between preeclampsia intervention and cancer therapy has been sought. Conclusions: Autophagy-based nanotechnology seems to be feasible in both placental ischemia in preeclampsia and cancers. This review draws parallels between targeted treatments in malignancies and placenta-derived PE. Comparing these diseases provides a novel molecular rationale and the possibility of identifying treatment through autophagy modulation.
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