MiR‐622 acts as a tumor suppressor to induce cell apoptosis and inhibit metastasis in human prostate cancer

Targhazeh, Niloufar; Yousefi, Bahman; Asghari, Samira; Mohammadnejhad, Reza; Mansouri, Parinaz; Valizadeh, Amir

doi:10.1111/and.14174

Cited by 9 publications

(5 citation statements)

References 40 publications

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“…37 miR-622 Open access also demonstrated as a tumor suppressor in some other human tumors, such as CRC, glioma, prostate cancer and renal cell carcinoma. [38][39][40][41] As a result, these data indicated that circ-0000512 knockdown might weaken TNBC progression and immune escape by promoting PD-L1 ubiquitination through sponging the miR-622/CMTM6 axis.…”

Section: Discussionmentioning

confidence: 79%

circ-0000512 inhibits PD-L1 ubiquitination through sponging miR-622/CMTM6 axis to promote triple-negative breast cancer and immune escape

Dong

Chen

Fan

et al. 2023

J Immunother Cancer

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BackgroundThis study reported the function and mechanism of circ-0000512 in the progression of triple-negative breast cancer (TNBC).Methodscirc-0000512 expression in TNBC tissues and paired adjacent normal tissues and cells was examined by qRT-PCR. Moreover, circ-0000512 expression in TNBC cells was modulated by transfection. Thereafter, colony formation assay, Transwell assay and flow cytometry were conducted to observe cell proliferation, migration and apoptosis. TNBC cells were treated with cycloheximide and the protease inhibitor MG132. Later, ubiquitination assay was performed to detect programmed cell death ligand 1 (PD-L1) ubiquitination in TNBC cells. The T cell killing ability was assessed by the T cell-mediated tumor cell killing assay. IFNγ and IL-2 levels were detected by ELISA. The percentage of activated T cells was detected with a flow cytometer. In addition, dual luciferase reporter gene assay and RNA immunoprecipitation assay were carried out to evaluate the binding between two genes. In vivo study was conducted on mice. CD8+ T cells in xenograft tumors were detected by immunohistochemistry.Resultscirc-0000512 was upregulated in patients with TNBC. circ-0000512 knockdown attenuated the proliferation and migration of TNBC cells and enhanced their apoptosis. circ-0000512 overexpression had opposite effects. circ-0000512 knockdown enhanced the PD-L1 protein ubiquitination in TNBC cells by inhibiting CMTM6. Meanwhile, circ-0000512 promoted CMTM6 expression by sponging miR-622. circ-0000512 knockdown increased the ratio of CD8+T cells and the lethality of T cells against TNBC cells. Besides, circ-0000512 knockdown inhibited the growth of TNBC cells in immunodeficient nude mice and normal immune mice and increased the ratio of CD8+T cells in xenograft tumors of normal immune mice.Conclusionscirc-0000512 inhibited PD-L1 ubiquitination by sponging the miR-622/CMTM6 axis, thus promoting TNBC progression and immune escape.

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Section: Discussionmentioning

confidence: 79%

circ-0000512 inhibits PD-L1 ubiquitination through sponging miR-622/CMTM6 axis to promote triple-negative breast cancer and immune escape

Dong

Chen

Fan

et al. 2023

J Immunother Cancer

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“…Furthermore, some patients suffer chemotherapy resistance, which, in some instances, is elucidated as tumor recurrence or progression [ 22 – 24 ]. It is essential to discern between two types of resistance: acquired and internal resistance [ 25 – 27 ]. Internal resistance is inherent as resistant cells exist within the tumor before initiating therapy.…”

Section: Discussionmentioning

confidence: 99%

Thymoquinone Increases the Sensitivity of SW‐480 Colon Cancer Cells to 5‐Fluorouracil

Zeinali,

Mahmoudzadeh,

Anarjani

et al. 2024

BioMed Research International

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Background: Studies have concentrated on the therapeutic potential of thymoquinone (TQ), a natural polyphenol, in diverse malignancies, such as colorectal cancer. Nevertheless, the precise mechanisms of TQ‐mediated anticancer properties are not yet fully elucidated.Objective: The present study has been designed to scrutinize the impact of TQ on 5‐fluorouracil (5‐FU)–mediated apoptosis in SW‐480 cells.Materials and Methods: SW‐480 cells were treated with TQ, 5‐FU, and a combination of TQ + 5‐FU. MTT assay was employed to assess cell viability. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was applied to evaluate apoptotic markers comprising Bcl‐2, Bax, and caspase‐9 expression levels. The γ‐H2AX protein expression was assessed by western blotting, and Annexin V flow cytometry was implemented to determine the apoptosis rate.Results: 5‐FU significantly reversed the cell proliferation in a dose‐dependent circumstance. The concurrent administration of TQ and 5‐FU led to a substantial inhibition of cell growth in comparison to single treatments (p < 0.05). TQ also facilitated apoptosis via upregulating Bax and caspase‐9 proapoptotic markers and suppressing antiapoptotic mediators, like Bcl‐2. In addition, TQ augmented 5‐FU‐induced apoptosis in SW‐480 cells. 5‐FU, combined with TQ, increased the protein expression of γ‐H2AX in SW‐480 cells compared with groups treated with TQ and 5‐FU alone.Conclusion: The present study’s findings unveil the significance of TQ as a potential therapeutic substance in colorectal cancer, particularly through enhancing 5‐FU‐induced apoptosis.

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“…Similarly, miRNAs have demonstrated predictive solid biomarker potential in PCa, and the dysregulation of these miRNA expressions is a hallmark of neoplasia formation and progression [14]. Though numerous miRNAs, such as miR-20b, miR-30, miR-32, miR-34, miR-199b, miR-210, miR-532, and miR-622 have been established to encourage or repress metastasis in PCa, many other miRNAs that play critical regulatory roles in metastasis have not yet been discovered [15][16][17][18][19][20]. MiR-32 is an intronic miRNA located in intron 14 of c9orf5, the gene encoding transmembrane protein 245 (TMEM245), on chromosome 9.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-32 Suppression: its Effects on Prostate Cancer Cells’ Capability to Proliferate and Migrate

et al. 2023

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Introduction This paper sought to scrutinize the role of microRNA-32 (miR-32) on the growth and migration as well as on the expression of metastatic genes in PC3 cells of prostate cancer in vitro. Methods Subsequent transfection of cells with miR-32 mimics, miR-32 inhibitor, negative control (NC), cell proliferation using MTT, and apoptosis by ELISA were performed. Furthermore, qRT-PCR was directed to measure the expression levels of matrix metalloproteinase 2 (MMP2) and vascular endothelial growth factors (VEGF) as metastatic and angiogenesis genes in the progression of PC3. Results miR-32 was overexpressed in PC3 cells compared to normal cells (P<0.001). Down-regulation of miR-32 obstructs in vitro proliferation and migration while intensifying the apoptosis rate in PC3 cells. Also, we found that miR-32 negatively modulates the expression of VEGF and MMP2 in PC3 cells. Conclusion These results indicate that the suppression of miR-32 might offer an auxiliary treatment procedure for addressing the invasion, progression, and metastasis in PCa patients by improving cell apoptosis.

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MiR‐622 acts as a tumor suppressor to induce cell apoptosis and inhibit metastasis in human prostate cancer

Cited by 9 publications

References 40 publications

circ-0000512 inhibits PD-L1 ubiquitination through sponging miR-622/CMTM6 axis to promote triple-negative breast cancer and immune escape

circ-0000512 inhibits PD-L1 ubiquitination through sponging miR-622/CMTM6 axis to promote triple-negative breast cancer and immune escape

Thymoquinone Increases the Sensitivity of SW‐480 Colon Cancer Cells to 5‐Fluorouracil

MicroRNA-32 Suppression: its Effects on Prostate Cancer Cells’ Capability to Proliferate and Migrate

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