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Abstract
Objective To investigate the effect of Rapamycin on proliferation and autophagy in human neuroblastoma (NB) cell lines and to elucidate the possible mechanism. Methods NB cells were treated with different concentrations of Rapamycin. Cell counting kit-8 (CCK-8) was used to measure proliferation, and flow cytometry (FCM) was used to analyze the cell cycle. EM was used to observe cell morphological changes. Western blotting (WB) was performed to detect the expression of Beclin-1, LC3-I/II, P62, mammalian target of Rapamycin (mTOR), and p-mTOR. Results Rapamycin inhibited the spread of NB cells in a dose- and time-dependent manner and arrested the cell cycle at the G0/G1 phase. EM showed autophagosomes in NB cells treated with Rapamycin. The WB results showed that the expression levels of Beclin-1 and LC3-II/LC3-I were significantly elevated in NB cells treated with Rapamycin, while the expression levels of P62, mTOR, and p-mTOR proteins were significantly reduced compared with the control cells (P<0.05). Conclusion Rapamycin inhibits cell proliferation and induces autophagy in human NB cell lines. The mechanism may be related to suppression of the mTOR signaling pathway.
Highlights
Neuroblastoma (NB) is the most well-known intracranial solid tumor in childhood, accounting for approximately 7–10% of all malignant tumors in children and is the most common extracranial solid tumor in children [1]
Rapamycin is a macrocyclic lactone isolated from Streptomyces hygroscopicus [17]
The present research mainly studied the effect of Rapamycin in human NB cell lines
Summary
Neuroblastoma (NB) is the most well-known intracranial solid tumor in childhood, accounting for approximately 7–10% of all malignant tumors in children and is the most common extracranial solid tumor in children [1] Multiple strategies, such as surgery, chemotherapy, radiotherapy, autologous stem cell transplantation, and various combinations of these therapies, have been used to treat NB [2]. Even with a series of progressive adjuvant therapies, the prognosis in late childhood is still poor, especially for children older than 1 year, and the long-term survival rate is still below 40% [3] This highlights the restrictions of existing treatment options and calls for more effective treatment strategies. The induction of autophagy is currently considered a novel therapeutic method
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