The targeting of non‑coding RNAs by curcumin: Facts and hopes for cancer therapy (Review)

Liu, Yun; Sun, Hongmei; Makabel, Bolat; Cui, Qingbin; Li, Jiajun; Su, Chaoyue; Ashby, Charles R.; Chen, Zhe‐Sheng; Zhang, Jianye

doi:10.3892/or.2019.7148

Cited by 30 publications

(35 citation statements)

References 120 publications

(125 reference statements)

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“…Plants have long been considered a rich source of bioactive natural products, some of which exhibit potent activity as potential anticancer agents (3)(4)(5)(6)(7). Costunolide is a sesquiterpene lactone (Fig.…”

Section: Introductionmentioning

confidence: 99%

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Wei

Qiu

et al. 2020

Oncol Rep

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Costunolide being a sesquiterpene lactone, is known to have anticancer properties. The present study investigated the anticancer effects of costunolide against the H1299 human non-small-cell lung cancer (NSCLC) cell line. Inhibition of cell viability by costunolide was assessed via a MTT assay. Furthermore, the apoptotic rate was detected using Annexin V/propidium iodide labeling. A colony forming cell assay was performed to investigate the antiproliferative effects of costunolide. Wound healing and Transwell assays were performed to determine the inhibitory effects of costunolide on migration and invasion, respectively. Western blot analysis was undertaken to determine protein expression, and reverse transcription-quantitative PCR was performed to assess mRNA expression levels. The results demonstrated that costunolide inhibited the viability of H1299 cells, with a half maximal inhibitory concentration value of 23.93±1.67 µM and induced cellular apoptosis in a dose-dependent manner. Furthermore, the colony formation, migrative and invasive abilities of the H1299 cells were inhibited in a dose-or time-dependent manner. The protein expression levels of E-cadherin increased and those of N-cadherin decreased following treatment with costunolide, which suggested that costunolide inhibited epithelial-to-mesenchymal transition. The mRNA levels of B-Raf, E-cadherin, N-cadherin, integrins α2 and β1, as well as matrix metalloproteinases 2 were also found to be regulated costunolide. These findings indicate the potential of costunolide in the treatment of NSCLC.

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Section: Introductionmentioning

confidence: 99%

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Wei

Qiu

et al. 2020

Oncol Rep

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“…The use of natural compounds and medicinal based plants for health promotion and adjuvant therapy is becoming increasingly popular worldwide (Li et al, 2019;Liu et al, 2019c). Zicao has been used as an effective treatment for a variety of inflammatory and infectious diseases for a long history.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the STAT3 Signaling Pathway Contributes to the Anti-Melanoma Activities of Shikonin

Cao

Liu

Lai³

et al. 2020

Front. Pharmacol.

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Background: Malignant melanoma is an extremely aggressive and metastatic cancer, and highly resistant to conventional therapies. Signal transducer and activator of transcription 3 (STAT3) signaling promotes melanoma development and progression, which has been validated as an effective target in melanoma treatment. Natural naphthoquinone shikonin is reported to exert anti-melanoma effects. However, the underlying mechanisms have not been fully elucidated. Purpose: This study aims to evaluate the anti-melanoma activities of shikonin and explore the involvement of STAT3 signaling in these effects. Methods: Zebrafish tumor model was established to evaluate the anti-human melanoma effects of shikonin in vivo. MTT assay and colony formation assay were employed to investigate the anti-proliferative effects of shikonin on human melanoma A375 and A2058 cells. Flow cytometry was used to analyze cell cycle distribution and apoptosis induction. Wound healing assay and Transwell chamber assay were conducted to examine the cell migratory and invasive abilities. Immunofluorescence assay was used to observe F-actin, Tubulin, and STAT3 localization. Western blotting was used to determine the expression levels of proteins associated with apoptosis and key proteins in the STAT3 signaling pathway. Immunoblotting was performed in DSS cross-linked cells to determine the homo-dimerization of STAT3. Gelatin zymography was employed to evaluate the enzymatic activity of MMP-2 and MMP-9. Transient transfection was used to overexpress STAT3 in cell models. Results: Shikonin suppressed melanoma growth in cultured cells and in zebrafish xenograft models. Shikonin induced melanoma cells apoptosis, inhibited cell migration and invasion. Mechanistic study indicated that shikonin inhibited the phosphorylation and homo-dimerization of STAT3, thus reduced its nuclear localization. Further study showed that shikonin decreased the levels of STAT3-targeted genes Mcl-1, Bcl-2, MMP-2,

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“…For example, in CRC, curcumin reversed oxaliplatin resistance via regulating the process of epithelial-mesenchymal transition [33]. What's more, Liu et al [34] reported that the regulatory effect of curcumin on LncRNAs in CRC. Therefore, we speculated that curcumin may reserve chemotherapy drug resistance in CRC via modulating LncRNAs.…”

Section: Discussionmentioning

confidence: 99%

LncRNA KCNQ1OT1 is a key factor in the reversal effect of curcumin on cisplatin resistance in the colorectal cancer cells

et al. 2020

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Context: The development of cisplatin resistance is a common cause of cancer recurrence in colorectal cancer (CRC). Long non-coding RNA KCNQ1OT1 has been proven to exert its oncogenic function in multiple cancers. Curcumin is a natural phenolic that could effectively suppress cisplatin resistance in CRC. Objective: To expound the role of KCNQ1OT1 in cisplatin resistance in CRC cells and whether KCNQ1OT1 participates in the reversal effect of curcumin on cisplatin resistance in CRC. Methods: Cell proliferation and apoptosis were evaluated by CCK-8 assay and ow cytometry assay, respectively. The interplay between KCNQ1OT1 and miR-497 was determined using RNA pull-down assay and dual-luciferase reporter gene assay. The combination of B-cell lymphoma 2 (Bcl-2) and miR-497 was con rmed using dual-luciferase reporter gene assay. Results: Compared with CRC cell line HCT8, the cisplatin-resistant CRC cell line HCT8/DDP exhibited a higher KCNQ1OT1 expression. Functionally, the silence of KCNQ1OT1 suppressed proliferation and promoted apoptosis in HCT8/DDP cells. KCNQ1OT1 could act as a sponge of miR-497 and removed the suppressive effect of miR-497 on Bcl-2 expression. Curcumin treatment suppressed proliferation and promote apoptosis in HCT8/DDP cells. While KCNQ1OT1 overexpression removed the effect of curcumin on HCT8/DDP cells via miR-497/ Bcl-2 axis. Finally, the in vivo experiments con rmed that the ectopic expression of KCNQ1OT1 reversed the suppressive effect of curcumin on the growth of cisplatin-resistant CRC cells. Conclusion: KCNQ1OT1 promoted cisplatin resistance in CRC cells via the miR-497/Bcl-2 axis. Administration of curcumin could effectively down-regulate KCNQ1OT1 expression, thus reversing cisplatin resistance in CRC cells.

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The targeting of non‑coding RNAs by curcumin: Facts and hopes for cancer therapy (Review)

Cited by 30 publications

References 120 publications

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Inhibition of the STAT3 Signaling Pathway Contributes to the Anti-Melanoma Activities of Shikonin

LncRNA KCNQ1OT1 is a key factor in the reversal effect of curcumin on cisplatin resistance in the colorectal cancer cells

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