AQP3 small interfering RNA and PLD2 small interfering RNA inhibit the proliferation and promote the apoptosis of squamous cell carcinoma

Wang, Xiaoyong; Tao, Chengjun; Yuan, Changzheng; Ren, Jin-ping; Yang, Ming; Ying, Hangyu

doi:10.3892/mmr.2017.6847

Cited by 13 publications

(8 citation statements)

References 33 publications

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“…For IHC analysis, glioma tissue sections were generated using polyformalin-fixed and paraffin-embedded tissues as previously described ( 32 ). The tissue sections were incubated with the primary monoclonal antibodies against KDELR2.…”

Section: Methodsmentioning

confidence: 99%

KDELR2 knockdown synergizes with temozolomide to induce glioma cell apoptosis through the CHOP and JNK/p38 pathways

Wang¹,

Cheng²,

Fan³

et al. 2021

Transl Cancer Res TCR

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Background: The C-terminal tetrapeptide Lys-Asp-Glu-Leu receptors (KDELRs) are transmembrane proteins that regulate ER stress (ERS) response, growth, differentiation, and immune responses. There is an association between KDELR2and promotion of glioblastoma tumorigenesis. The aim of the present study was to explore the functional mechanism of KDELR2 in glioma and during response to chemotherapy to temozolomide (TMZ).Methods: The expression of KDELR2 in glioma tissues and cells was evaluated by immunohistochemistry, western blot and RT-qPCR assay. Then role of KDELR2 was demonstrated by CCK8, colony formation, flow cytometry and Hochest 33258 assays. The expression of genes (ATF4, ATF6, PERK, eIF2-α, GRP78 and CHOP) in U373 cells was evaluated by RT-qPCR. The protein expression of genes (cleaved caspase 3, caspase 3, cleaved PARP, PARP, Bax, Bcl-2, JNK, p-JNK, p38, p-p38, ATF4, ATF6, XBP-1s, PERK, p-PERK, GRP78 and CHOP) was measured by western blot assay.Results: The expression of KDELR2 was upregulated in high-grade gliomas tissues. KDELR2 knockdown suppressed cell proliferation but increased cell apoptosis. Further, Knockdown of KDELR2 also activated the ER stress (ERS)-dependent CHOP pathway, and resulted in increased levels of phosphorylated c-Jun N-terminal kinase (JNK) and p38. Moreover, the combination of KDELR2 knockdown and TMZ application showed a synergistic cytotoxic effect in U373 cells through the ERS-dependent CHOP and JNK/p38 pathways.Conclusions: KDELR2 knockdown induces apoptosis and sensitizes glioma cells to TMZ, which is mediated by the ERS-dependent CHOP and JNK/p38 pathways.

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Section: Methodsmentioning

confidence: 99%

KDELR2 knockdown synergizes with temozolomide to induce glioma cell apoptosis through the CHOP and JNK/p38 pathways

Wang¹,

Cheng²,

Fan³

et al. 2021

Transl Cancer Res TCR

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“…Wang et al . elucidated that AQP3 promoted cell proliferation and enhanced cell apoptosis in squamous cell carcinoma . Additionally, Muhammad et al .…”

Section: Introductionmentioning

confidence: 95%

miR‐874 directly targets AQP3 to inhibit cell proliferation, mobility and EMT in non‐small cell lung cancer

Wang

Yang

et al. 2020

Thoracic Cancer

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Background: Non-small cell lung cancer (NSCLC) is a major type of lung cancer with high morbidity and high mortality. miR-874 has been determined to play a role in tumor suppression in several cancers. The purpose of our study was to detect the biological mechanisms of miR-874 and AQP3 in NSCLC. Methods: CCK-8 and Transwell assays were utilized to perform cell invasion. Western blot was employed to evaluate the protein expression. Results: The expression of miR-874 was lower in NSCLC tissues than that of corresponding adjacent nontumor tissues. Downregulation of miR-874 predicted a poor prognosis in NSCLC. The cell proliferation and mobility were suppressed by overexpression of miR-874, which were promoted by knockdown of miR-874 in A549 and H1299 cells. miR-874 mediated the expression of AQP3 by directly binding to the 3 0 -untranslated regions (UTR) of AQP3 mRNA in NSCLC cells. Moreover, miR-874 inhibited the proliferation and mobility by targeting AQP3 and inhibited the PI3K/AKT signaling pathway in A549 cells. miR-874 inhibited the growth of NSCLC in vivo. Conclusions:In conclusion, miR-874 inhibited proliferation and mobility by regulating AQP3 in NSCLC. The newly identified miR-874/AQP3 axis provides novel insight into the pathogenesis of NSCLC.

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“…Cancer stem cells (CSCs) maintain the stemness to ensure their survival and growth, and becoming resistant to current treatments [14][15][16]. The intrinsic pathway of CD133 + Huh7 cells is regulated by the AQP3 protein in the progression and metastasis of several malignant tumors [17][18][19][20]. Furthermore, Nek2 is the critical regulator of the centrosome, making hepatocellular carcinoma more resistance to current treatments [21,22].…”

Section: Introductionmentioning

confidence: 99%

A novel nitidine chloride nanoparticle overcomes the stemness of CD133+EPCAM+ Huh7 hepatocellular carcinoma cells for liver cancer therapy

Li¹,

Zhang²,

Zhou³

et al. 2022

BMC Pharmacol Toxicol

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Background Stemness of CD133+EPCAM+ hepatocellular carcinoma cells ensures cancer resistance to apoptosis,which is a challenge to current liver cancer treatments. In this study, we evaluated the tumorcidal activity of a novel nanoparticle of nitidine chloride (TPGS-FA/NC, TPGS-FA: folic acid modified D-α-tocopheryl polyethylene glycol 1000 succinate, NC: nitidine chloride), against human hepatocellular carcinoma (HCC) cell line Huh7 growth in vitro and in vivo. Methods Huh7 cells were treated with TPGS-FA/NC. Cell proliferation was assessed using MTT and colony assays. The expression of cell markers and signaling proteins was detected using western blot analyses. A sphere culture technique was used to enrich cancer stem cells (CSC) in Huh7 cells. TPGS-FA/NC (7.5, 15, 30, 60, 120 μg/mL) dose-dependently inhibited the proliferation of HCC cells, which associated with a reduction in AQP3 and STAT3 expression. Importantly,TPGS-FA/NC (10, 20, and 40 μg/mL) significantly reduced the EpCAM+/CD133+cell numbers, suppressed the sphere formation. The in vivo antitumor efficacy of TPGS-FA/NC was proved in Huh7 cell xenograft model in BALB/c nude mice, which were administered TPGS-FA/NC(4 mg· kg − 1· d − 1, ig) for 2 weeks. Results TPGS-FA/NC dose-dependently suppressed the AQP3/STAT3/CD133 axis in Huh7 cells. In Huh7 xenograft bearing nude mice, TPGS-FA/NC administration markedly inhibited Huh7 xenograft tumor growth . Conclusions TPGS-FA/NC inhibit HCC tumor growth through multiple mechanisms, and it may be a promising candidate drug for the clinical therapy of hepatocellular carcinoma.

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AQP3 small interfering RNA and PLD2 small interfering RNA inhibit the proliferation and promote the apoptosis of squamous cell carcinoma

Cited by 13 publications

References 33 publications

KDELR2 knockdown synergizes with temozolomide to induce glioma cell apoptosis through the CHOP and JNK/p38 pathways

KDELR2 knockdown synergizes with temozolomide to induce glioma cell apoptosis through the CHOP and JNK/p38 pathways

miR‐874 directly targets AQP3 to inhibit cell proliferation, mobility and EMT in non‐small cell lung cancer

A novel nitidine chloride nanoparticle overcomes the stemness of CD133+EPCAM+ Huh7 hepatocellular carcinoma cells for liver cancer therapy

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