Beneficial effect of fluoxetine on anti-tumor progression on hepatocellular carcinoma and non-small cell lung cancer bearing animal model

Hsu, Li-Cho; Tu, Hsi-Feng; Hsu, Fei‐Ting; Yueh, Po-Fu; Chiang, I-Tsang

doi:10.1016/j.biopha.2020.110054

Cited by 34 publications

(37 citation statements)

References 48 publications

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“…Hsu et al con rmed via in vivo experiments that uoxetine in hepatocellular carcinoma (HCC) and NSCLC can signi cantly reduce tumor cell proliferation, induce apoptosis, and regulate the expression of invasion-related proteins. Its potential mechanism of action in two tumors may be by blocking the activation of Akt/NF-κB or Erk/NF-κB signaling pathways [77]. MUN et al also supported the conclusion that Fluoxetine plays an anti-tumor role in HCC [78].…”

Section: Discussionmentioning

confidence: 96%

Identification of a novel small nucleolar RNAs prognostic signature for patients with acute myelocytic leukemia

Huang¹,

Liao²,

Li³

2020

Preprint

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Background: This study mainly used The Cancer Genome Atlas (TCGA) RNA sequencing dataset to screen prognostic snoRNAs of acute myeloid leukemia (AML), and used for the construction of prognostic snoRNAs signature for AML. Methods: A total of 130 AML patients with RNA sequencing dataset were used for prognostic snoRNAs screenning. SnoRNAs co-expressed genes and differentially expressed genes (DEGs) were used for functional annotation, as well as gene set enrichment analysis (GSEA). Connectivity Map (CMap) also used for potential targeted drugs screening. Results:Through genome-wide screening, we identified 30 snoRNAs that were significantly associated with the prognosis of AML. Then we used the step function to screen a prognostic signature composed of 14 snoRNAs (SNORD72, SNORD38, U3, SNORA73B, SNORD79, SNORA73, SNORD12B, SNORA74, SNORD116-12, SNORA65, SNORA14, snoU13, SNORA75, SNORA31), which can significantly divide AML patients into high- and low-risk groups. Through GSEA, snoRNAs co-expressed genes and DEGs functional enrichment analysis, we screened a large number of potential functional mechanisms of this prognostic signature in AML, such as phosphatidylinositol 3-kinase-Akt ,Wnt, epithelial to mesenchymal transition, T cell receptors, NF-kappa B, mTOR and other classic cancer-related signaling pathways. In the subsequent targeted drug screening using CMap, we also identified six drugs that can be used for AML targeted therapy, they were alimemazine, MG-262, fluoxetine, quipazine, naltrexone and oxybenzone. Conclusion: Our current study was constructed an AML prognostic signature based on the 14 prognostic snoRNAs, which may serve as a novel prognostic biomarker for AML.

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Section: Discussionmentioning

confidence: 96%

Identification of a novel small nucleolar RNAs prognostic signature for patients with acute myelocytic leukemia

Huang¹,

Liao²,

Li³

2020

Preprint

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“…Consistent with a previous study ( 17 ), the current study demonstrated that emodin suppressed PCNA expression in TPC-1 cells. Cell cycle interruption is a major feature of tumor transformation and the status of the cell cycle represents a prognostic index for cancer ( 18 ). Cyclin-D1, which is a regulator of the G 1 /S cell cycle, serves an essential role in tumor progression, contributes to tumor growth and resists anticancer drugs ( 18 ).…”

Section: Discussionmentioning

confidence: 99%

“…Cell cycle interruption is a major feature of tumor transformation and the status of the cell cycle represents a prognostic index for cancer ( 18 ). Cyclin-D1, which is a regulator of the G 1 /S cell cycle, serves an essential role in tumor progression, contributes to tumor growth and resists anticancer drugs ( 18 ). It was therefore hypothesized that emodin would reduce the expression of Cyclin-D1 expression in TPC-1 cells and in a xenograft model.…”

Section: Discussionmentioning

confidence: 99%

Emodin inhibits the proliferation of papillary thyroid carcinoma by activating AMPK

Wang

et al. 2021

Exp Ther Med

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Emodin has been demonstrated to serve antitumor roles in a variety of tumor types, but the effect of emodin on papillary thyroid carcinoma and its molecular mechanisms remain unclear.In the current study, the role of emodin on papillary thyroid carcinoma was analyzed in vitro and in vivo. TPC-1 cells were treated with emodin (0, 10, 25 or 50 µM), and cell viability and apoptosis were detected using Cell Counting Kit-8 and flow cytometry, respectively. The expression levels of AMPK-associated proteins were examined using western blot analysis. To study the effect of emodin on the AMPK pathway, AMPK activator, AICAR and an AMPK inhibitor, Dorsomorphin, were used in TPC-1 cells. In vivo, mice were used to confirm the mechanism of emodin on papillary thyroid carcinoma. The results of the current study indicated that emodin treatment induced cell apoptosis and cell cycle arrest in TPC-1 cells. Furthermore, the inhibitory effect increased in a dose dependent manner. Following emodin treatment, the cell viability of TPC-1 cells was significantly decreased, and apoptosis rate increased (P<0.05). Furthermore, the expression levels of AMPK were increased in the emodin group compared with the control group (P<0.05). Similar effects were observed following AMPK activator treatment in TPC-1 cells. Following AMPK activator treatment, cell proliferation and the cell cycle were inhibited. Also, the AMPK inhibitor was demonstrated to mediate the therapeutic effect of emodin. In addition, the results of the present study demonstrated that emodin inhibited the MEK/ERK pathway. Additionally, the in vivo results of the current study were consistent with those in vitro. In conclusion, the current study demonstrated that the administration of Emodin inhibited the proliferation of papillary thyroid cancer cells via activating AMPK pathway activity.

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“…Depression is frequently found in the cancer patients, with higher prevalence than general population 24 . Antidepressants are the common drugs to cure depression and also have the anticancer effect 25 . However, different antidepressants may have different impact on tumors.…”

Section: Discussionmentioning

confidence: 99%

Antidepressants Fluoxetine Mediates Endoplasmic Reticulum Stress and Autophagy of Non-Small Cell Lung Cancer Cells Through ATF4-AKT-mTOR Signaling Pathway.

Shao

Zhuang

et al. 2021

Preprint

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Cancer patients often suffer the depression with worse quality of life and prognosis. Therefore, studying how antidepressants affect the cancer is of great significance. Recent years witnessed the reports that antidepressants have the antiproliferation effect, However, in lung cancer it’s still unclear about the specific molecular target. This study mainly focused on how fluoxetine influenced different types of cells and discovered the molecular basis of its inhibitory effect in lung cancer. The specific antiproliferation effect and autophagy induced by fluoxetine on lung cancer cell were shown in CCK8 and immunofluorescence. The RNA sequence hinted that the endoplasmic reticulum (ER) stress-related protein and mTOR pathway were enriched after fluoxetine treating. Western blot results revealed that the ER stress pathway was activated by fluoxetine, including PERK, ATF4, and CHOP, while the AKT/mTOR pathway was inhibited. In addition, the transfection of ATF4 siRNA further discovered that ER stress participated in the inhibition of AKT/mTOR pathway and the induction of antiproliferation and autophagy in the fluoxetine-treated cells. More importantly, fluoxetine was demonstrated to play cytotoxic activity in cancer cells without affecting normal cells. Our results showed that fluoxetine triggered the ATF4-AKT-mTOR signaling pathway to induce cell cycle arrest and autophagy restraining cancer cells’ growth in lung cancer. This study found fluoxetine unaffected the proliferation of normal lung epithelial cells, providing safe clinical therapeutic strategies for lung cancer patients with depression.

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Beneficial effect of fluoxetine on anti-tumor progression on hepatocellular carcinoma and non-small cell lung cancer bearing animal model

Cited by 34 publications

References 48 publications

Identification of a novel small nucleolar RNAs prognostic signature for patients with acute myelocytic leukemia

Identification of a novel small nucleolar RNAs prognostic signature for patients with acute myelocytic leukemia

Emodin inhibits the proliferation of papillary thyroid carcinoma by activating AMPK

Antidepressants Fluoxetine Mediates Endoplasmic Reticulum Stress and Autophagy of Non-Small Cell Lung Cancer Cells Through ATF4-AKT-mTOR Signaling Pathway.

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