Curcumin regulates the miR-21/PTEN/Akt pathway and acts in synergy with PD98059 to induce apoptosis of human gastric cancer MGC-803 cells

Qiang, Zhanrong; Meng, Lingyu; Yi, Caixia; Yu, Lianying; Chen, Wenxia; Sha, Wei

doi:10.1177/0300060518822213

Cited by 52 publications

(32 citation statements)

References 29 publications

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“…Overall, these results suggested that the miR-21/PTEN pathway mediated geniposide-induced cardioprotection against ox-LdL injury. In addition, studies have demonstrated the roles of the miR-21/PTEN pathway in tumor growth, migration and invasion (44,45). combined with previous studies regarding the protection of geniposide against tumor (15,46), miR-21/PTEN pathway may contribute to the antitumor effect of geniposide.…”

Section: Discussionmentioning

confidence: 83%

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

et al. 2020

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Oxidized low-density lipoprotein (ox-LdL)-induced vascular endothelial damage, oxidative stress and inflammation play a vital role in the pathophysiology of atherosclerosis. Geniposide is the primary active ingredient from Gardenia jasminoides Ellis associated with anti-oxidative properties and cardioprotective action. However, the therapeutic mechanism of geniposide in atherosclerosis remains unclear. Hence, the present study aimed to elucidate the underlying mechanisms of geniposide in oxidative stress and inflammatory response during ox-LdL injury in human umbilical vein endothelial cells (HUVEcs), focusing particularly on the microRNA (miR)-21/PTEN pathway. The results demonstrated that geniposide pretreatment significantly increased cell viability, decreased lactate dehydrogenase release, increased miR-21 level and decreased PTEN expression under ox-LdL condition. Subsequently, transfection with miR-21 mimic enhanced the protection of geniposide on ox-LdL-induced cytotoxicity and apoptosis (mediated by the upregulation of apoptotic rate and caspase-3 activity), whereas miR-21 inhibitor reversed these effects of geniposide. In addition, geniposide resulted in an anti-oxidant effect as evidenced by the decrease in reactive oxygen species generation, malondialdehyde content and NAdPH oxidase 2 expression, and the increase in superoxide dismutase, glutathione peroxidase and catalase activities in ox-LdL-treated HUVEcs, which were exacerbated by miR-21 mimic and reversed by miR-21 inhibitor. Furthermore, geniposide mitigated the ox-LdL-induced inflammatory response, demonstrated by a downregulation of pro-inflammatory cytokine (IL-1β, IL-6, and TNF-α) levels and an upregulation of anti-inflammatory cytokine (IL-10) level. However, miR-21 mimic enhanced, whereas miR-21 inhibitor attenuated, these effects of geniposide. In conclusion, the present results indicated that geniposide protects HUVEcs from ox-LdL injury by inhibiting oxidative stress and inflammation, and that these effects are partly due to the enhancement of the miR-21/PTEN pathway.

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Section: Discussionmentioning

confidence: 83%

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

et al. 2020

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“…The anticancer effect of curcumin was considered to inhibit cell proliferation by suppressing multiple cell signaling pathways (8). For example, curcumin could induce apoptosis by regulating the miR-21/PTEN/AKT signaling pathway in MGC-803 cells (9). Furthermore, curcumin inhibited cell migration and invasion by regulating miR-99a and JAK/STAT signaling pathway in retinoblastoma cells (10).…”

mentioning

confidence: 99%

Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway

et al. 2020

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Curcumin has been proved to inhibit cell proliferation and induce cell apoptosis in non-small cell lung cancer (NSCLC). However, little is known about antimetastatic effects and molecular mechanisms of curcumin in NSCLC. In this study, we investigated the involvement of miR-206 in curcumin’s anti-invasion and anti-migration in NSCLC. Cell proliferation was determined by MTT assay. Cell migration and invasion were analyzed by wound healing assay and transwell assay. MiRNA-206 expression was detected by real-time PCR. Western blot was used to detect the protein expression of PI3K/AKT/mTOR signaling pathway. Curcumin significantly inhibited migration and invasion in A549 cells, accompanied by significantly elevated miR-206 expression. Overexpression of miR-206 could inhibit migration and invasion of A549 cells, but it could also significantly decrease the phosphorylation levels of mTOR and AKT. The inhibition of miR-206 promoted cell migration, invasion and increased the phosphorylation level of mTOR and AKT. Furthermore, miR-206 mimics improved the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT in A549 cells. On the contrary, MiR-206 inhibitors reversed the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT. In conclusion, curcumin inhibited cell invasion and migration in NSCLC by elevating the expression of miR-206 which further suppressed the activation of the PI3K/AKT/mTOR pathway.

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“…Administration of curcumin (5–40 μM) reduces expression of miR-21 to activate PTEN signaling (highest effect in high doses of curcumin). Then, Akt undergoes downregulation to suppress proliferation of GC cells [ 188 ]. To date, just one study has evaluated the efficacy of curcumin in targeting PTEN signaling in GC cells, and more studies will reveal different molecular pathways of curcumin action in targeting PTEN in GC cells.…”

Section: Antitumor Compounds Target Ptenmentioning

confidence: 99%

PTEN, a Barrier for Proliferation and Metastasis of Gastric Cancer Cells: From Molecular Pathways to Targeting and Regulation

et al. 2020

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Cancer is one of the life-threatening disorders that, in spite of excellent advances in medicine and technology, there is no effective cure for. Surgery, chemotherapy, and radiotherapy are extensively applied in cancer therapy, but their efficacy in eradication of cancer cells, suppressing metastasis, and improving overall survival of patients is low. This is due to uncontrolled proliferation of cancer cells and their high migratory ability. Finding molecular pathways involved in malignant behavior of cancer cells can pave the road to effective cancer therapy. In the present review, we focus on phosphatase and tensin homolog (PTEN) signaling as a tumor-suppressor molecular pathway in gastric cancer (GC). PTEN inhibits the PI3K/Akt pathway from interfering with the migration and growth of GC cells. Its activation leads to better survival of patients with GC. Different upstream mediators of PTEN in GC have been identified that can regulate PTEN in suppressing growth and invasion of GC cells, such as microRNAs, long non-coding RNAs, and circular RNAs. It seems that antitumor agents enhance the expression of PTEN in overcoming GC. This review focuses on aforementioned topics to provide a new insight into involvement of PTEN and its downstream and upstream mediators in GC. This will direct further studies for evaluation of novel signaling networks and their targeting for suppressing GC progression.

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Curcumin regulates the miR-21/PTEN/Akt pathway and acts in synergy with PD98059 to induce apoptosis of human gastric cancer MGC-803 cells

Cited by 52 publications

References 29 publications

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

miR‑21/PTEN pathway mediates the cardioprotection of geniposide against oxidized low‑density�lipoprotein‑induced endothelial injury via suppressing oxidative stress and inflammatory response

Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway

PTEN, a Barrier for Proliferation and Metastasis of Gastric Cancer Cells: From Molecular Pathways to Targeting and Regulation

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