RBCK1 contributes to chemoresistance and stemness in colorectal cancer (CRC)

Liu, Minli; Zang, Feng; Zhang, Shengjun

doi:10.1016/j.biopha.2019.109250

Cited by 55 publications

(44 citation statements)

References 39 publications

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“…Chemotherapy is an inevitable part of cancer therapy, but its potential has been restricted in recent years, due to the resistance of cancer cells [ 259 , 260 ]. In fact, chemoresistance of cancer cells has urged scientists to seek new anti-tumor agents [ 261 ].…”

Section: Chrysin Chemotherapy and Drug Resistancementioning

confidence: 99%

Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives

et al. 2020

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Pharmacological profile of phytochemicals has attracted much attention to their use in disease therapy. Since cancer is a major problem for public health with high mortality and morbidity worldwide, experiments have focused on revealing the anti-tumor activity of natural products. Flavonoids comprise a large family of natural products with different categories. Chrysin is a hydroxylated flavonoid belonging to the flavone category. Chrysin has demonstrated great potential in treating different disorders, due to possessing biological and therapeutic activities, such as antioxidant, anti-inflammatory, hepatoprotective, neuroprotective, etc. Over recent years, the anti-tumor activity of chrysin has been investigated, and in the present review, we provide a mechanistic discussion of the inhibitory effect of chrysin on proliferation and invasion of different cancer cells. Molecular pathways, such as Notch1, microRNAs, signal transducer and activator of transcription 3 (STAT3), nuclear factor-kappaB (NF-κB), PI3K/Akt, MAPK, etc., as targets of chrysin are discussed. The efficiency of chrysin in promoting anti-tumor activity of chemotherapeutic agents and suppressing drug resistance is described. Moreover, poor bioavailability, as one of the drawbacks of chrysin, is improved using various nanocarriers, such as micelles, polymeric nanoparticles, etc. This updated review will provide a direction for further studies in evaluating the anti-tumor activity of chrysin.

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Section: Chrysin Chemotherapy and Drug Resistancementioning

confidence: 99%

Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives

et al. 2020

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“…To generate tumor xenografts, EpCAM + CD44 + HCT-116 cells (5×10 5 ) were injected subcutaneously into the right ank of each mouse. When the mice attained a tumor volume of 40-60 mm 3 , they were randomly divided into 3 groups (n = 10) and treated with Nanog siRNA, mock, or negative siRNA control. Nanog siRNA or negative siRNA control was injected intratumorally twice a week for 3 weeks.…”

Section: In Vivo Tumor Xenograft Assaymentioning

confidence: 99%

“…Taken together, these results demonstrate that Nanog siRNA treatment suppresses colorectal tumor growth in vivo and improves survival, implying that Nanog may serve as a novel therapeutic target for CRC treatment. For survival analysis, mice were sacri ced when tumors measured > 2000 mm 3 or the tumor diameter exceeded 2.0 cm. All of the treatments with mice are according to the protocol of the Animal Care Committee of Jilin University as previously described [20].…”

Section: Nanog Silencing Decreases the Invasive Ability Of Ccscs In Vmentioning

confidence: 99%

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RNAi mediated silencing of Nanog expression suppresses the growth of human colorectal cancer stem cells

Zhang

Zhao

Yang

et al. 2020

Preprint

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Background: Colorectal cancer (CRC) is the third most common cancer in the world known for its poor recurrence-free prognosis. Previous studies have shown that it is closely linked with cancer stem cells (CSCs), which have self-renewal potential and the capacity to differentiate into diverse populations. Nanog is an important transcription factor that functions to maintain the self-renewal and proliferation of embryonic stem cells; however, many recent studies have shown that Nanog is also highly expressed in many cancer stem cells. Methods: To investigate whether Nanog plays a crucial role in maintaining the stemness of colorectal CSCs (CCSCs), RNA interference was used to downregulate Nanog expression in the CRC stem cell line, EpCAM + CD44 + HCT-116. We examined the anti-tumor function of Nanog in vitro and in vivo, using small interfering RNA. Results: Our results revealed that the Nanog mRNA expression level in CCSCs was higher than that in HCT-116 cells. We found that the depletion of Nanog inhibited proliferation and promoted apoptosis in EpCAM + CD44 + HCT-116 cells. In addition, the invasive ability of EpCAM + CD44 + HCT-116 cells was markedly restricted when Nanog was silenced by small interfering RNA. Furthermore, we found that the silencing of Nanog decreased tumor size and weight and improved the survival rate of tumor-bearing mice. Conclusions: In conclusion, these findings collectively demonstrate that Nanog, which is highly expressed in CRC stem cells, is a key factor in the development of tumor growth, and it may serve as a potential marker of prognosis and a novel and effective therapeutic target for the treatment of CRC.

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“…Accumulating evidences suggest that chemosensitivity of tumor cells is closely related to their stemness characteristics (4,13,14). For this, we next examined the potential involvement of LINC00680 in HCC sensitivity to chemotherapeutic agents, such as 5-Fluorouracil (5-Fu), in vitro and in vivo.…”

Section: Linc00680 Promotes Hcc Cell Stemness and Increase Hcc Chemormentioning

confidence: 99%

LINC00680 Enhances Hepatocellular Carcinoma Stemness Behavior and Chemoresistance by Sponging miR-568 to Upregulate AKT3

Shu

Wang

et al. 2020

Preprint

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Background: Hepatocellular carcinoma (HCC) has an extremely poor prognosis due to the development of chemoresistance, coupled with inherently increased stemness properties. Long non-coding RNAs (LncRNAs) are key regulators for tumor cell stemness and chemosensitivity. Currently the relevance between LINC00680 and tumor progression was still largely unknown, with only one study showing its significance in glioblastoma. The study herein was aimed at identifying the role of LINC00680 in the regulation HCC stemness and chemosensitivity. Methods: QRT-PCR was used to detect the expression of LINC00680, miR-568 and AKT3 in tissue specimen and cell lines. Gain- or loss-of function assays were applied to access the function of LINC00680 in HCC cells, including cell proliferation and stemness properties. HCC stemness and chemosensitivity were determined by sphere formation, cell viability and colony formation. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull down assays were performed to examine the interaction between LINC00680 and miR-568 as well as that between miR-568 and AKT3. A nude mouse xenograft model was established for the in vivo study.Results: We found that LINC00680 was remarkably upregulated both in HCC tissue and cell lines. Patients with high level of LINC00680 had poorer prognosis. LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Mechanism study revealed that LINC00680 regulated HCC stemness and chemosensitivity through sponging miR-568, thereby expediting the expression of AKT3, which further activated its downstream signaling molecules, including mTOR, elF4EBP1, and p70S6K.Conclusion: LINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3, suggesting that LINC00680 might be a potentially important HCC diagnosis marker and therapeutic target.

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RBCK1 contributes to chemoresistance and stemness in colorectal cancer (CRC)

Cited by 55 publications

References 39 publications

Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives

Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives

RNAi mediated silencing of Nanog expression suppresses the growth of human colorectal cancer stem cells

LINC00680 Enhances Hepatocellular Carcinoma Stemness Behavior and Chemoresistance by Sponging miR-568 to Upregulate AKT3

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