Alantolactone sensitizes human pancreatic cancer cells to EGFR inhibitors through the inhibition of STAT3 signaling

Zheng, Hailun; Yang, Lehe; Kang, Yanting; Chen, Min; Lin, Shichong; Xiang, Youqun; Li, Caleb; Dai, Xuanxuan; Huang, Xiaoying; Liang, Guang; Zhao, Chengguang

doi:10.1002/mc.22951

Cited by 47 publications

(48 citation statements)

References 40 publications

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“…alT is the main biologically active compound derived from Inula helenium (42). alT has been widely researched as a potential candidate for the treatment of several types of cancer, and previous in vivo studies have reported its antiproliferative, anti-metastatic and anti-invasive activity in a variety of cell lines (19,20,42). The present study aimed to evaluate the effect of alT on osteosarcoma and to determine whether it could be used as a potential future treatment strategy for this disease.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported that alT promotes numerous biological effects, including anti-inflammatory and antioxidant functions (18,19). it has also been observed to suppress several types of human cancer, including gastric, pancreatic and breast cancer cells (19)(20)(21). it is reported that these anticancer effects of alT are mediated through the Pi3K/aKT signaling pathway (22).…”

Section: Introductionmentioning

confidence: 99%

“…alantolactone (alT) is a biologically natural compound derived from Inula helenium (17). Previous studies have reported that alT promotes numerous biological effects, including anti-inflammatory and antioxidant functions (18,19). it has also been observed to suppress several types of human cancer, including gastric, pancreatic and breast cancer cells (19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

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Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway

et al. 2019

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osteosarcoma is the most common type of malignant bone cancer and results in cancer-related deaths among adolescents. alantolactone (alT) demonstrates antitumor properties in various diseases; however, its potential role in osteosarcoma is relatively unclear. The aim of the present study was to evaluate the effect of alT on osteosarcoma. alT significantly decreased the viability of U2OS and HOS osteosarcoma cell lines. Cells flow cytometry assay and Hoechst 33258 staining assay revealed that ALT significantly increased the proportion of apoptotic u2oS cells. in addition, wound healing and Transwell invasion assays demonstrated that the invasion and migration of osteosarcoma were markedly reduced upon alT treatment. it was hypothesized that the antitumor functions of alT are mediated through inhibition of the Pi3K/aKT signaling pathway. in conclusion, the results of the present study confirmed the inhibition of ALT on osteosarcoma cells via downregulation of Pi3K/aKT signaling pathways, suggesting alT as a potential therapeutic candidate for osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway

et al. 2019

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“…Cao et al stated that ALT may improve the therapeutic e ciency of the chemotherapeutic drug oxaliplatin [10]. Zheng et al demonstrated that ALT could sensitize human pancreatic cancer cells to EGFR inhibitors [11]. The anti-tumor properties of ALT have been shown to occur through a range of molecular mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Alantolactone inhibits cell autophagy and promotes apoptosis via AP2M1 in acute lymphoblastic leukemia

Shi

Lan

Wang

et al. 2020

Preprint

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Background: Acute lymphoblastic leukemia (ALL) is an aggressive hematopoietic malignancy that is most commonly observed in children. Alantolactone (ALT) has been reported to exhibit anti-tumor activity in different types of cancer. The aim of the present study was to investigate the anti-tumor activity and molecular mechanism of ALT in ALL. Methods: ALL cell lines were treated with 1, 5 and 10 μM ALT, and cell viability was assessed using an MTT assay and RNA sequencing. Flow cytometry, JC-1 staining and immunofluorescence staining assays were used to measure cell apoptosis and autophagy. Additionally, western blot analysis was used to detect expression of apoptosis and autophagy related proteins. Finally, the effects of ALT on tumor growth were assessed in a BV173 xenograft nude mouse model. Results: ALT inhibited the proliferation of ALL cells in a dose-dependent manner. Additionally, it was demonstrated that ALT inhibited cell proliferation, colony formation, autophagy, induced apoptosis and reduced tumor growth in vivo through upregulating the expression of adaptor related protein complex 2 subunit mu 1 (AP2M1). Moreover, the autophagy activator rapamycin, attenuated the pro-apoptotic effects of ALT on BV173 and NALM6 cell lines. Overexpression of AP2M1 decreased the expression of Beclin1 and the LC3-II/LC3-1 ratio, and increased p62 expression. Knockdown of Beclin1 increased the levels of bax, cleaved caspase 3 and cytochrome C, and decreased bcl-2 expression. Conclusions: The present study demonstrated that ALT exerts anti-tumor activity through inducing apoptosis and inhibiting autophagy by upregulating AP2M1 in ALL, highlighting a potential therapeutic strategy for treatment of ALL.

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“…Although some STAT3 inhibitors are undergoing clinical trials, none of the STAT3 inhibitors have been approved to date for the treatment of cancer . Accordingly, there is an urgent need to discover new drugs that can act as STAT3 inhibitors, either alone or in combination with the currently available anticancer drugs to address the unmet clinical need …”

Section: Introductionmentioning

confidence: 99%

Aminocyanopyridines as anti‐lung cancer agents by inhibiting the STAT3 pathway

Qiu

Yang

et al. 2019

Molecular Carcinogenesis

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Lung cancer is a leading cause of cancer-related death worldwide. Cyanopyridines and aminocyanopyridines with carbon-nitrogen bonds have been proved to exert significant anticancer, antibacterial, and anti-inflammatory effects. In this study, we showed that aminocyanopyridine 3o and 3k displaying potent antitumor activity via inhibiting the signal transducer and activator of transcription 3 (STAT3) pathway. They blocked the constitutive STAT3 phosphorylation in a dose-and time-dependent manner and regulated the transcription of STAT3 target genes encoding apoptosis factors. Most importantly, 3o also inhibited interleukin-6-induced STAT3 activation and nuclear localization. Furthermore, 3o significantly inhibited the tumor growth of H460-derived xenografts. Taken together, these findings suggest that 3o and 3k are promising therapeutic drug candidates for lung cancer by inhibiting persistent STAT3 signaling.

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Alantolactone sensitizes human pancreatic cancer cells to EGFR inhibitors through the inhibition of STAT3 signaling

Cited by 47 publications

References 40 publications

Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway

Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway

Alantolactone inhibits cell autophagy and promotes apoptosis via AP2M1 in acute lymphoblastic leukemia

Aminocyanopyridines as anti‐lung cancer agents by inhibiting the STAT3 pathway

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