MiR-28-5p mediates the anti-proliferative and pro-apoptotic effects of curcumin on human diffuse large B-cell lymphoma cells

Tian, Kui; Sun, Wei‐Zen; Lü, Xiaofei; Wang, Xinliang; Lian, Jiqin

doi:10.1177/0300060520943792

Cited by 8 publications

(6 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, miR-28-5p inhibited cell proliferation and migration in Renal Cell Carcinoma by directly inhibiting the Rap1b gene [ 41 ]. The miR-28-5p was also reported to inhibit cell growth and promote apoptosis of DLBCL cells through Curcumin [ 42 ]. Studies have also found that miR-28-5p was upregulated in some tumors, implying their critical role in tumor metastasis and invasion [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of hsa-miR-28-5p on Adriamycin Sensitivity in Diffuse Large B-Cell Lymphoma

Yan

Shang

Hai-peng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Background. Adriamycin (doxorubicin) is an important traditional drug that exhibits cytotoxicity in Diffuse Large B-cell Lymphoma (DLBCL). Doxorubicin affects the DLBCL cells at all stages of their cell cycle. Combined with our previous results, this study discovered that the overexpression of hsa-miR-28-5p inhibited the proliferation, promoted apoptosis, and triggered cell cycle arrest at the S-phase in DLBCL cells. However, the effect of (Homo sapiens, hsa)-microRNA (miR)-28-5p on doxorubicin sensitivity in DLBCL has not been investigated. This study aims to reveal the effects of hsa-miR-28-5p on doxorubicin sensitivity at the level of DLBCL cells. Methods. To determine the optimal concentration of doxorubicin, different concentrations of doxorubicin were used to treat DLBCL cells. CCK-8 assay was used to detect the proliferation of DLBCL cells. The hsa-miR-28-5p-mimic NC and hsa-miR-28-5p mimic were transfected to doxorubicin-mediated DLBCL cells. Simultaneously, blank control groups were set up. The cells were cultured and transfected for 24 h. Next, each group was administered with different concentrations of doxorubicin and cultured again for 24 h to observe the effects of hsa-miR-28-5p on doxorubicin sensitivity at different times. The proliferation, early apoptosis, and late apoptosis in DLBCL cells were determined using soft agar colony-forming assay, mitochondrial membrane potential assay, and caspase-3 activity assay, respectively. The apoptosis and cell cycle were explored using Annexin V-PE/7-AAD and PI/RNase staining buffer, respectively. We speculated that PD-L1 might be involved in the effect of hsa-miR-28-5p on the sensitivity of adriamycin (doxorubicin) in the DLBCL cells. Hence, we performed immunohistochemistry (IHC) to determine PD-L1 expression within formalin-fixed paraffin-embedded (FFPE) samples from 52 DLBCL cases. Results. The optimal concentration of doxorubicin targeting DLBCL cells was found to be 3.028 μmol/l. The effect of doxorubicin on DLBCL cells was time- and concentration-dependent. hsa-miR-28-5p mimic + doxorubicin remarkably decreased proliferation of DLBCL. DLBCL cell apoptosis rate was the highest in hsa-miR-28-5p mimic + doxorubicin group. Apart from that, hsa-miR-28-5p mimic plus doxorubicin had the best effect in promoting DLBCL cell apoptosis. After the intervention of hsa-miR-28-5p mimic + doxorubicin on DLBCL cells, the cell cycle was arrested in the S-phase and DNA synthesis was blocked. hsa-miR-28-5p mimic + doxorubicin could regulate the cycle of DLBCL cells. As a result, overexpression of hsa-miR-28-5p combined with doxorubicin is possibly involved in the development of DLBCL by affecting the proliferation, apoptosis, and cycle of DLBCL cells. PD-L1 showed an association with the prognosis of DLBCL patients. Combining with the literature, this suggested hsa-miR-28-5p may influence DLBCL occurrence and therapeutic effect by regulating the PD-L1 level. Conclusion. The combination of hsa-miR-28-5p mimic and doxorubicin may be considered more effective in inhibiting growth, arresting the cell cycle, and promoting cell apoptosis of DLBCL cells compared to using doxorubicin alone. The effects of doxorubicin on DLBCL cells were found to be time- and concentration-dependent. The overexpression of hsa-miR-28-5p enhanced the effect of doxorubicin on DLBCL cells, which may be attributed to the regulation of PD-L1 levels.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of hsa-miR-28-5p on Adriamycin Sensitivity in Diffuse Large B-Cell Lymphoma

Yan

Shang

Hai-peng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

show abstract

“…By increasing miRNA-28–5p expression, curcumin reduces BECN1 expression and enhances p62 expression. 96 Curcumin-mediated lncRNA regulation has been also reported. Briefly, lncRNAs are similar to miRNAs in terms of inability in encoding proteins and both of them have regulatory functions in cells.…”

Section: Curcumin and Lymphomamentioning

confidence: 98%

“… 95 Curcumin suppresses progression and survival of lymphoma cells. 96 miRNA-28–5p is another factor involved in regulating progression of lymphoma. miRNA-28–5p has poor expression in lymphoma and its upregulation suppresses tumor progression via YWHAZ down-regulation.…”

Section: Curcumin and Lymphomamentioning

confidence: 99%

Curcumin in treatment of hematological cancers: Promises and challenges

Entezari,

Tayari,

Paskeh

et al. 2024

Journal of Traditional and Complementary Medicine

View full text Add to dashboard Cite

“…A detailed investigation of ferroptosis responses for these natural products and miRNAs is warranted. Curcumin [272] miR-125b-5p PEITC [273], quercetin [274], EGCG [275], berberine [276] miR-1287-5p Curcumin [277] miR-129-5p Matrine [278] miR-142-3p Artesunate [279], quercetin [280], curcumin [281] miR-143-3p Curcumin [282], EGCG [283,284], sulforaphane [285], quercetin [286] miR-144-3p Curcumin [287] miR-15a-5p Curcumin [288], baicalin [289], Withaferin A [290] miR-15a-3p EGCG [284] miR-205-5p Cryptotanshinone ↓ [291] proanthocyanidins ↓ [292], curcumin [293] miR-214-3p EGCG [284], sulforaphane [285] miR-25-3p Withaferin A [294] miR-27a-3p β-elemene [295], quercetin [296] miR-28-5p Curcumin [297] miR-302a-3p Curcumin [298] miR-324-3p Salinomycin ↓ [299] miR-365a-3p Sulforaphane [300] miR-375-3p Solasonine [301] miR-409-3p Curcumin [302] miR-429 Curcumin [303], berberine ↓ [304,305] miR-489-3p Curcumin [306] Ferroptosisinhibiting miRNAs miR-18a-5p Curcumin ↓ [307] miR-19a-3p Berberine [308], proanthocyanidins …”

Section: Ferroptosis-modulating Mirnas Are Associated With Some Natur...mentioning

confidence: 99%

“…Ferroptosis-inducing natural products, such as curcumin, sulforaphane, and solasonine, are associated with upregulating ferroptosis-inducing miRNAs ( Table 4 ). Curcumin induces the antiproliferation and apoptosis of large B-cell lymphoma cells by upregulating miR-28-5p, which is reversed by miR-28-5p inhibition [ 297 ]. Similarly, curcumin inhibits the proliferation and EMT gene expression of colon cancer cells by inducing miR-302a-3p expression [ 298 ].…”

Section: Ferroptosis-modulating Mirnas Are Associated With Some Natur...mentioning

confidence: 99%

Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis

Chuang,

Yen,

Chien

et al. 2024

IJMS

View full text Add to dashboard Cite

Ferroptosis, which comprises iron-dependent cell death, is crucial in cancer and non-cancer treatments. Exosomes, the extracellular vesicles, may deliver biomolecules to regulate disease progression. The interplay between ferroptosis and exosomes may modulate cancer development but is rarely investigated in natural product treatments and their modulating miRNAs. This review focuses on the ferroptosis-modulating effects of natural products and miRNAs concerning their participation in ferroptosis and exosome biogenesis (secretion and assembly)-related targets in cancer and non-cancer cells. Natural products and miRNAs with ferroptosis-modulating effects were retrieved and organized. Next, a literature search established the connection of a panel of ferroptosis-modulating genes to these ferroptosis-associated natural products. Moreover, ferroptosis-associated miRNAs were inputted into the miRNA database (miRDB) to bioinformatically search the potential targets for the modulation of ferroptosis and exosome biogenesis. Finally, the literature search provided a connection between ferroptosis-modulating miRNAs and natural products. Consequently, the connections from ferroptosis–miRNA–exosome biogenesis to natural product-based anticancer treatments are well-organized. This review sheds light on the research directions for integrating miRNAs and exosome biogenesis into the ferroptosis-modulating therapeutic effects of natural products on cancer and non-cancer diseases.

show abstract

MiR-28-5p mediates the anti-proliferative and pro-apoptotic effects of curcumin on human diffuse large B-cell lymphoma cells

Cited by 8 publications

References 40 publications

Effects of hsa-miR-28-5p on Adriamycin Sensitivity in Diffuse Large B-Cell Lymphoma

Effects of hsa-miR-28-5p on Adriamycin Sensitivity in Diffuse Large B-Cell Lymphoma

Curcumin in treatment of hematological cancers: Promises and challenges

Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis

Contact Info

Product

Resources

About