Recent nanotechnological interventions targeting PI3K/Akt/mTOR pathway: A focus on breast cancer

Sharma, Varruchi; Sharma, Anil Kumar; Punj, Vasu; Panneerselvam, Priya

doi:10.1016/j.semcancer.2019.08.005

Cited by 55 publications

(39 citation statements)

References 134 publications

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“…Extracellular HMGB1 mediates various responses by interacting with its cell surface receptors and triggering diverse biological effects, such as cell proliferation, migration, differentiation and apoptosis [30,31]. Akt/mTOR and ERK signalling pathways play an important role in cell proliferation, survival, growth and apoptosis [32][33][34]. We examined the effects of HMGB1 on Akt/mTOR and ERK/CREB signalling pathway activation.…”

Section: Discussionmentioning

confidence: 99%

High mobility group box 1 regulates gastric cancer cell proliferation and migration via RAGE-mTOR/ERK feedback loop

Tang¹,

Wang²,

Cai

et al. 2021

J. Cancer

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Gastric cancer (GC) is a common malignancy tumour in China. Despite various therapeutic approaches to improve the survival rate of GC patients, the effectiveness of currently available treatments remains unsatisfactory. High mobility group box 1 (HMGB1) is reported to play a role in tumour development. However, the molecular mechanisms involved in HMGB1-mediated regulation of proliferation and migration of GC cells remain unclear. In the present study, we demonstrated that HMGB1 is highly expressed in GC cells and tissue. In HGC-27 GC cells, HMGB1 overexpression or HMGB1 RNA interference both demonstrated that HMGB1 could promote GC cell proliferation and migration. Investigation of the underlying molecular mechanisms revealed that HMGB1 enhanced cyclins expression, induced epithelial-to-mesenchymal transition and matrix metalloproteinase (MMPs) expression and promoted RAGE expression as well as RAGE-mediated activation of Akt/mTOR/P70S6K and ERK/P90RSK/CREB signalling pathways. We also found that inhibition of ERK and mTOR using specific inhibitors reduced recombinant human HMGB1-induced RAGE expression, suggesting that the RAGE-mTOR/ERK positive feedback loop is involved in HMGB1-induced GC cell proliferation and migration. Our study highlights a novel mechanism by which HMGB1 promotes GC cell proliferation and migration via RAGE-mediated Akt-mTOR and ERK-CREB signalling pathways which also involves the RAGE-mTOR/ERK feedback loop. These findings indicate that HMGB1 is a potential therapeutic target for GC.

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Section: Discussionmentioning

confidence: 99%

High mobility group box 1 regulates gastric cancer cell proliferation and migration via RAGE-mTOR/ERK feedback loop

Tang¹,

Wang²,

Cai

et al. 2021

J. Cancer

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“…Hyperactivation of PI3K/AKT pathway is involved in the progression of breast cancer and contributes to the poor outcome [22]. Our results found that lower DTX1 expression was associated with higher cancer cell proliferation and increased invasion and metastasis, and moreover these findings were related with PI3K/AKT pathway.…”

Section: Discussionmentioning

confidence: 48%

Deltex1 promotes cell proliferation and invasion and associated with clinical characteristics of breast cancer

wang

Liu

et al. 2020

Preprint

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Background Deltex1 (DTX1) was found to play its role in the development of several kinds of cancer. The association between DTX1 and breast cancer was unclear. We aimed to investigate the association between DTX1 expression and clinical characteristics of breast cancer, further explore the possible mechanisms of DTX1 on the development of breast cancer. Methods We determined level of DTX1 expression by qRT-PCR, analyzed association between DTX1 and clinical characteristics of breast cancer by student’s test and ANOVA test. The possible mechanisms of DTX1 on the development of breast cancer were explored with breast cancer cell lines in vitro. Results Levels of DTX1 in breast cancer tissues were lower compared to FCD tissues and peri-neoplastic breast tissues (P<0.01). Lower expression of DTX1 was associated with advanced tumor grade (grade III, P=0.002), advanced clinical TNM stage (III-IV stage, P=0.017), positive lymph node metastasis (P=0.034) and high Ki-67 index (P=0.031). Multivariate Cox regression analysis revealed that DTX1 expression was recognized as an independent prognostic factor for MFS in breast cancer. Elevated levels of Notch1, Jagged1 and HES1 in NOTCH pathway and p-Akt/PKB in PI3K/AKT pathway were found in breast cancer cells with lower DTX1 expression. GSI treatment could inhibit breast cancer cell proliferation and migration through NOTCH/DTX1/PI3K/AKT pathways. Conclusion Lower DTX1 in breast tissues was associated with advanced condition, prognosis and metastasis of breast cancer. Lower DTX1 might promote breast cancer cell proliferation and migration via NOTCH/DTX1/PI3K/AKT pathways. DTX1 might be useful as a marker to select new therapy for breast cancer.

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“…The AKT-mTOR signaling pathway has been reported to regulate numerous cellular processes, such as cell growth, proliferation and migration [13,14]. When analysis the relationship between the AKT-mTOR signaling pathway and miR-18a-3p, we found that AKT-mTOR signaling pathway were associated with miR-18a-3p expression (Fig.…”

Section: Hht Inhibited Breast Cancer Cells Growth Via Mir-18a-3p-akt-mentioning

confidence: 75%

Homoharringtonine inhibited breast cancer cells growth via miR-18a-3p/AKT/mTOR signaling pathway

Wang

et al. 2021

Int. J. Biol. Sci.

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Homoharringtonine (HHT), a natural alkaloid derived from the cephalotaxus, exhibited its anti-cancer effects in hematological malignancies clinically. However, its pesticide effects and mechanisms in treating solid tumors remain unclear. In this study, we found that HHT was capable of inhibiting tumor growth after 5-days treatment of breast cancer cells, MCF-7, in vivo. Furthemore, HHT also significantly inhibited the cancer cell growth and induced cell apoptosis in vitro. miRNA sequencing proved miR-18a-3p was noticeably downregulated in the cells after HHT treatment. Moreover, downregulating miR-18a-3p increased HHT-induced cell apoptosis; our data supported that HHT suppressed miR-18a-3p expression and inhibited tumorigenesis might via AKT-mTOR signaling pathway. In conclusion: our study proved that HHT suppressed breast cancer cell growth and promoted apoptosis mediated by regulating of the miR-18a-3p-AKT-mTOR signaling pathway, HHT may be a promising antitumor agent in breast cancer treatment.

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Recent nanotechnological interventions targeting PI3K/Akt/mTOR pathway: A focus on breast cancer

Cited by 55 publications

References 134 publications

High mobility group box 1 regulates gastric cancer cell proliferation and migration via RAGE-mTOR/ERK feedback loop

High mobility group box 1 regulates gastric cancer cell proliferation and migration via RAGE-mTOR/ERK feedback loop

Deltex1 promotes cell proliferation and invasion and associated with clinical characteristics of breast cancer

Homoharringtonine inhibited breast cancer cells growth via miR-18a-3p/AKT/mTOR signaling pathway

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