Hypoxia‐induced SM22α in A549 cells activates the IGF1R/PI3K/Akt pathway, conferring cellular resistance against chemo‐ and radiation therapy

Kim, Tae Rim; Cho, Eun Wie; Paik, Sang Gi; Kim, In Gyu

doi:10.1016/j.febslet.2011.12.036

Cited by 43 publications

(45 citation statements)

References 26 publications

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“…Several studies have shown that AKT is activated by hypoxia in various tumor types [17,23,38,41,45,46]. We have also observed phosphorylated AKT(Ser473) expression specifically in hypoxic areas of head and neck cancer xenografts and patient biopsies ( Fig.…”

Section: Pi3-k/akt Pathway and Hypoxia-induced Signalingsupporting

confidence: 67%

“…These HIF-1-inducible genes regulate a multitude of cellular processes, including cell proliferation, angiogenesis, glucose metabolism, and apoptosis [36]. All these cellular processes are important for resistance to both chemotherapy and radiotherapy [38][39][40][41][42]. In addition to HIF-1, hypoxia signaling is mediated via the unfolded protein response (UPR) and the Fig.…”

Section: Hypoxia-related Treatment Resistancementioning

confidence: 99%

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Improving chemoradiation efficacy by PI3-K/AKT inhibition

Stegeman¹,

Span²,

Kaanders³

et al. 2014

Cancer Treatment Reviews

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Section: Pi3-k/akt Pathway and Hypoxia-induced Signalingsupporting

confidence: 67%

Section: Hypoxia-related Treatment Resistancementioning

confidence: 99%

Improving chemoradiation efficacy by PI3-K/AKT inhibition

Stegeman¹,

Span²,

Kaanders³

et al. 2014

Cancer Treatment Reviews

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“…There is a strong link of rapidly altered metabolic activity induced by target inhibition of the IGF-1R signaling pathways in proliferating cells. Through direct interaction with IGF1Rβ, SM22α overexpression enhances tumor cell growth and activates the IGF1R/PI3K/Akt pathway [30,31]. Our results show that IGF2R also regulates cell proliferation, apoptosis, migration, and invasive ability.…”

Section: Discussionmentioning

confidence: 79%

IGF2R Expression is Associated with the Chemotherapy Response and Prognosis of Patients with Advanced NSCLC

Tian¹,

Yao²,

Song³

et al. 2014

Cell Physiol Biochem

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Background: Insulin-like growth factor (IGF) pathway has been suggested as a new molecular target for the treatment of cancer including Non-small cell lung cancer (NSCLC). We postulated that IGF-2 receptor (IGF2R) may be associated with treatment response and prognosis of NSCLC patients receiving chemotherapy. Methods: A total of 464 patients with inoperable advanced stage of NSCLC were enrolled. All patients received platinum-based chemotherapy. Meanwhile, the IGF2R expression in tumor samples was detected by Immunohistochemical analysis. The IGF2R expression was inhibited in several human NSCLC cell lines (H292, A549, NCI-H460, Calu-3 and NCI-H23) after small interfering RNA (siRNA) transfection and the cellular biology behavior were evaluated. Results: Of all NSCLC patients, 204 had high IGF2R expression and 260 had low IGF2R expression. The low IGF2R expression was significantly associated with the smoking status, higher tumor stage, and poorer differentiation status of these patients. Notably, we found that the low IGF2R expression was closely associated with the chemotherapy response in NSCLC patients. Patients with low IGF2R expressions had a poorer prognosis than those with high IGF2R expressions. IGF2R inhibition by si-RNA technique in NSCLC cell lines increased the proliferation, migration and invasion abilities, but reduced the apoptosis rate. IGF2R silencing significantly enhanced the chemo-resistance of NSCLC cell lines to cisplatin treatment. Conclusion: The IGF2R expression in tumor is associated with the chemotherapy response and prognosis of Patients with advanced NSCLC.

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“…Moreover, SAA also changes EMT markers and inhibits transgelin 2 expression. There is strong evidence in the literature of a link between chemoresistance and EMT, which is a critical event in cancer development 22 was also found to be associated with the growth of lung cancer cells 28 . Consistent with these findings, our previous study showed that transgelin 2 was critically involved in the growth of MCF-7/PTX cells 13 transgelin 2 by SAA is likely to be a safer approach for the treatment of breast cancer.…”

Section: Knockdown Of Transgelin 2 Inhibited Paclitaxel Resistance Mmentioning

confidence: 99%

Salvianolic acid A reverses the paclitaxel resistance and inhibits the migration and invasion abilities of human breast cancer cells by inactivating transgelin 2

Zheng

Chen

Yang

et al. 2015

Cancer Biology & Therapy

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Multidrug resistance and tumor migration and invasion are the major obstacles to effective breast cancer chemotherapy, but the underlying molecular mechanisms remain unclear. This study investigated the potential of transgelin 2 and salvianolic acid A to modulate the resistance and the migration and invasion abilities of paclitaxel-resistant human breast cancer cells (MCF-7/PTX). MCF-7/PTX cells were found to exhibit not only a high degree of resistance to paclitaxel, but also strong migration and invasion abilities. Small interfering RNA-mediated knockdown of TAGLN2 sensitized the MCF-7/PTX cells to paclitaxel, and inhibited their migration and invasion abilities. In addition, we also observed that combined salvianolic acid A and paclitaxel treatment could reverse paclitaxel resistance, markedly inhibit tumor migration and invasion, and suppress the expression of transgelin 2 in MCF-7/PTX cells. These findings indicate that salvianolic acid A can reverse the paclitaxel resistance and inhibit the migration and invasion abilities of human breast cancer cells by down-regulating the expression of transgelin 2, and hence could be useful in breast cancer treatments.

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Hypoxia‐induced SM22α in A549 cells activates the IGF1R/PI3K/Akt pathway, conferring cellular resistance against chemo‐ and radiation therapy

Cited by 43 publications

References 26 publications

Improving chemoradiation efficacy by PI3-K/AKT inhibition

Improving chemoradiation efficacy by PI3-K/AKT inhibition

IGF2R Expression is Associated with the Chemotherapy Response and Prognosis of Patients with Advanced NSCLC

Salvianolic acid A reverses the paclitaxel resistance and inhibits the migration and invasion abilities of human breast cancer cells by inactivating transgelin 2

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