MicroRNA‑29c restores cisplatin sensitivity in liver cancer through direct inhibition of sirtuin 1 expression

Zhang, Wei; Luo, Peng

doi:10.3892/ol.2018.8801

Cited by 3 publications

(2 citation statements)

References 42 publications

(42 reference statements)

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“…miR-29c was previously reported to play a tumor-suppressive role by targeting key pathways in cancer and CSC population [ 49 , 50 ]. Furthermore, ectopic miR-29c expression sensitizes cancer cells to paclitaxel chemotherapy [ 51 ]. Similarly, ID2 expression in cancer is also correlated with self-renewal ability and resistance to chemotherapy [ 52 , 53 ], suggesting the significance of miR-29c and ID2 axis in cancer.…”

Section: Discussionmentioning

confidence: 99%

LncRNA IPW inhibits growth of ductal carcinoma in situ by downregulating ID2 through miR-29c

Deshpande

Sharma²,

Yin

et al. 2022

Breast Cancer Res

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Background Ductal carcinoma in situ (DCIS) of breast is the noninvasive lesion that has propensity to progress to the malignant form. At present, it is still unknown which lesions can potentially progress to invasive forms. In this study, we aimed to identify key lncRNAs involved in DCIS growth. Methods We employ disease-related lncProfiler array to identify IPW in specimens of DCIS and matching control samples and validate the observations in three DCIS-non-tumorigenic cell lines. Further, we examine the mechanism of IPW action and the downstream signaling in in vitro and in vivo assays. Importantly, we screened a library containing 390 natural compounds to identify candidate compound selectively inhibiting IPW low DCIS cells. Results We identified lncRNA IPW as a novel tumor suppressor critical for inhibiting DCIS growth. Ectopic expression of IPW in DCIS cells strongly inhibited cell proliferation, colony formation and cell cycle progression while silencing IPW in primary breast cells promoted their growth. Additionally, orthotropic implantation of cells with ectopic expression of IPW exhibited decreased tumor growth in vivo. Mechanistically, IPW epigenetically enhanced miR-29c expression by promoting H3K4me3 enrichment in its promoter region. Furthermore, we identified that miR-29c negatively regulated a stemness promoting gene, ID2, and diminished self-renewal ability of DCIS cells. Importantly, we screened a library containing 390 natural compounds and identified toyocamycin as a compound that selectively inhibited the growth of DCIS with low expression of IPW, while it did not affect DCIS with high IPW expression. Toyocamycin also suppressed genes associated with self-renewal ability and inhibited DCIS growth in vivo. Conclusion Our findings revealed a critical role of the IPW-miR-29c-ID2 axis in DCIS formation and suggested potential clinical use of toyocamycin for the treatment of DCIS.

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Section: Discussionmentioning

confidence: 99%

LncRNA IPW inhibits growth of ductal carcinoma in situ by downregulating ID2 through miR-29c

Deshpande

Sharma²,

Yin

et al. 2022

Breast Cancer Res

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“…Finally, miR-362 and miR-505 overexpression were observed in gastric cancer cells ( Xia et al, 2014 ; Wang Z. et al, 2020 ), and their enhanced expression promoted nuclear accumulation of NF-κB/p65, due to both miRs targeted CYLD directly and its downregulation mediated NF-κB activation. Besides, Zhang and Luo found that miR-29c was downregulated in HepG2/DDP cells, and demonstrated that miR-29c targeted SIRT1 ( Zhang and Luo, 2018 ). SIRT1 may have enhanced activity in tumor cell growth by promoting NF-κB expression ( Yeung et al, 2004 ).…”

Section: Micrornas Involved In Ddp-chemoresistancementioning

confidence: 99%

Contribution of MicroRNAs in Chemoresistance to Cisplatin in the Top Five Deadliest Cancer: An Updated Review

Loren

Saavedra

et al. 2022

Front. Pharmacol.

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Cisplatin (DDP) is a well-known anticancer drug used for the treatment of numerous human cancers in solid organs, including bladder, breast, cervical, head and neck squamous cell, ovarian, among others. Its most important mode of action is the DNA-platinum adducts formation, inducing DNA damage response, silencing or activating several genes to induce apoptosis; these mechanisms result in genetics and epigenetics modifications. The ability of DDP to induce tumor cell death is often challenged by the presence of anti-apoptotic regulators, leading to chemoresistance, wherein many patients who have or will develop DDP-resistance. Cancer cells resist the apoptotic effect of chemotherapy, being a problem that severely restricts the successful results of treatment for many human cancers. In the last 30 years, researchers have discovered there are several types of RNAs, and among the most important are non-coding RNAs (ncRNAs), a class of RNAs that are not involved in protein production, but they are implicated in gene expression regulation, and representing the 98% of the human genome non-translated. Some ncRNAs of great interest are long ncRNAs, circular RNAs, and microRNAs (miRs). Accumulating studies reveal that aberrant miRs expression can affect the development of chemotherapy drug resistance, by modulating the expression of relevant target proteins. Thus, identifying molecular mechanisms underlying chemoresistance development is fundamental for setting strategies to improve the prognosis of patients with different types of cancer. Therefore, this review aimed to identify and summarize miRs that modulate chemoresistance in DDP-resistant in the top five deadliest cancer, both in vitro and in vivo human models.

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The role of SIRT1 in autophagy and drug resistance: unveiling new targets and potential biomarkers in cancer therapy

Tang,

Ju,

Liu

et al. 2024

Front. Pharmacol.

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Cancer, the world’s second leading cause of death after cardiovascular diseases, is characterized by hallmarks such as uncontrolled cell growth, metastasis, angiogenesis, hypoxia, and resistance to therapy. Autophagy, a cellular process that can both support and inhibit cancer progression, plays a critical role in cancer development and progression. This process involves the formation of autophagosomes that ultimately fuse with lysosomes to degrade cellular components. A key regulator of this process is Sirtuin 1 (SIRT1), which significantly influences autophagy. This review delves into the role of SIRT1 in modulating autophagy and its broader impacts on carcinogenesis. SIRT1 regulates crucial autophagy mediators, such as AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR), effectively promoting or suppressing autophagy. Beyond its direct effects on autophagy, SIRT1’s regulatory actions extend to other cell death processes, including apoptosis and ferroptosis, thereby influencing tumor cell proliferation, metastasis, and chemotherapy responses. These insights underscore the complex interplay between SIRT1 and autophagy, with significant implications for cancer therapy. Targeting SIRT1 and its associated pathways presents a promising strategy to manipulate autophagy in cancer treatment. This review underscores the potential of SIRT1 as a therapeutic target, opening new avenues for enhancing cancer treatment efficacy.

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MicroRNA‑29c restores cisplatin sensitivity in liver cancer through direct inhibition of sirtuin 1 expression

Cited by 3 publications

References 42 publications

LncRNA IPW inhibits growth of ductal carcinoma in situ by downregulating ID2 through miR-29c

LncRNA IPW inhibits growth of ductal carcinoma in situ by downregulating ID2 through miR-29c

Contribution of MicroRNAs in Chemoresistance to Cisplatin in the Top Five Deadliest Cancer: An Updated Review

The role of SIRT1 in autophagy and drug resistance: unveiling new targets and potential biomarkers in cancer therapy

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