Endoplasmic reticulum stress induces 5-fluorouracil resistance in human colon cancer cells

Kim, Joon Ki; Kang, Kyoung Ah; Piao, Mei Jing; Ryu, Yea Seong; Han, Xiaodong; Fernando, Pattage Madushan Dilhara Jayatissa; Oh, Min Chang; Park, Jeong Eon; Shilnikova, Kristina; Boo, Sun Jin; Na, Soo‐Young; Jeong, Young Jin; Jeong, Seung Uk; Hyun, Jin Won

doi:10.1016/j.etap.2016.05.005

Cited by 37 publications

(20 citation statements)

References 32 publications

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“…In LoVo colon cancer cells, 5-FU negatively affected CRC growth by increasing ROS generation, causing ER stress, which, in turn, induced cell apoptosis. In addition, higher levels of GRP78 production in cancer cells is known to produce ER-stress tolerance because GRP78 is a calciumbinding molecular chaperone located in the ER that works to maintain ER homeostasis and suppresses stress-induced apoptosis (32,33). Thus, our results demonstrated that in combination with 5-FU, down-regulation of GRP78 in LoVo cancer cells led to higher generation of ROS and ER stress level (Figures 2-4).…”

Section: Effect Of Glucose-regulated Protein (Grp78) Silencing On 5-fmentioning

confidence: 57%

Enhanced Susceptibility to 5-Fluorouracil in Human Colon Cancer Cells by Silencing of GRP78

Yun

Han

Lee

et al. 2017

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Section: Effect Of Glucose-regulated Protein (Grp78) Silencing On 5-fmentioning

confidence: 57%

Enhanced Susceptibility to 5-Fluorouracil in Human Colon Cancer Cells by Silencing of GRP78

Yun

Han

Lee

et al. 2017

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“…Then, the UPR would attenuates ER stress mediated by taxane so that tumor cells could survive from the taxane treatment. Besides, Kim et al [29] found that ER stress induced 5-fluoropyrimidines resistance in human colon cancer cells and Yun et al [30] found that down-regulation of GRP78 could lead to enhanced sensitivity of cancer cells to cytotoxic effect of 5-fluoropyrimidines [30]. Therefore, we considered that AGR3 could promote sensitivity of breast cancer cells to 5-fluoropyrimidines also due to the interaction with GRP78.…”

Section: Discussionmentioning

confidence: 96%

Anterior Gradient 3 Promotes Breast Cancer Development and Chemotherapy Response

Shao

Zhang

et al. 2020

Cancer Res Treat

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Anterior gradient 3 (AGR3) belongs to human anterior gradient (AGR) family. The function of AGR3 on cancer remains unknown. This research aimed to investigate if AGR3 had prognostic values in invasive ductal carcinoma (IDC) of breast cancer and could promote tumor progression. Materials and Methods AGR3 expression was detected in breast benign lesions, ductal carcinoma in situ and IDC by immunohistochemistry analysis. AGR3's correlations with clinicopathological features and prognosis of IDC patients were analyzed. By cell function experiments, collagen gel droplet-embedded culture drug sensitivity test and cytotoxic analysis, AGR3's impacts on proliferation, invasion ability, and chemotherapeutic drug sensitivity of breast cancer cells were also detected. Results AGR3 was up-regulated in luminal subtype of histological grade I-II of IDC patients and positively correlated with high risks of recurrence and distant metastasis. AGR3 high expression could lead to bone or liver metastasis and predict poor prognosis of luminal B. In cell lines, AGR3 could promote proliferation and invasion ability of breast cancer cells which were consistent with clinical analysis. Besides, AGR3 could indicate poor prognosis of breast cancer patients treated with taxane but a favorable prognosis with 5-fluoropyrimidines. And breast cancer cells with AGR3 high expression were resistant to taxane but sensitive to 5-fluoropyrimidines. Conclusion AGR3 might be a potential prognostic indicator in luminal B subtype of IDC patients of histological grade I-II. And patients with AGR3 high expression should be treated with chemotherapy regimens consisting of 5-fluoropyrimidines but no taxane.

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“…Harnessing the adaptive power of the UPR is one mechanism exploited by cancer cells to ensure survival upon exposure to chemotherapeutic agents, with all three arms of the UPR being implicated (Figure ). Knockdown of GRP78, ATF6, ATF4 and XBP1s has been linked to the resensitisation of chemoresistant cells [Wang et al., ; Kim et al., ; Chen et al., ]. XBP1s has been implicated in promoting relapse of TNBC tumours in vivo .…”

Section: Upr and Chemoresistancementioning

confidence: 99%

The role of the unfolded protein response in cancer progression: From oncogenesis to chemoresistance

Madden

Logue

Healy

et al. 2018

Biology of the Cell

256

187

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Tumour cells endure both oncogenic and environmental stresses during cancer progression. Transformed cells must meet increased demands for protein and lipid production needed for rapid proliferation and must adapt to exist in an oxygen‐ and nutrient‐deprived environment. To overcome such challenges, cancer cells exploit intrinsic adaptive mechanisms such as the unfolded protein response (UPR). The UPR is a pro‐survival mechanism triggered by accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER), a condition referred to as ER stress. IRE1, PERK and ATF6 are three ER anchored transmembrane receptors. Upon induction of ER stress, they signal in a coordinated fashion to re‐establish ER homoeostasis, thus aiding cell survival. Over the past decade, evidence has emerged supporting a role for the UPR in the establishment and progression of several cancers, including breast cancer, prostate cancer and glioblastoma multiforme. This review discusses our current knowledge of the UPR during oncogenesis, tumour growth, metastasis and chemoresistance.

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Endoplasmic reticulum stress induces 5-fluorouracil resistance in human colon cancer cells

Cited by 37 publications

References 32 publications

Enhanced Susceptibility to 5-Fluorouracil in Human Colon Cancer Cells by Silencing of GRP78

Enhanced Susceptibility to 5-Fluorouracil in Human Colon Cancer Cells by Silencing of GRP78

Anterior Gradient 3 Promotes Breast Cancer Development and Chemotherapy Response

The role of the unfolded protein response in cancer progression: From oncogenesis to chemoresistance

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