E-cadherin increasing multidrug resistance protein 1 via hypoxia-inducible factor-1α contributes to multicellular resistance in colorectal cancer

Liu, Xi; Xu, Xueqing; Wang, Fengchao; Ni, Li; He, Jia

doi:10.1007/s13277-015-3811-6

Cited by 18 publications

(39 citation statements)

References 34 publications

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“…In a similar approach, Luebke-Wheeler, Nedredal, Yee, Amiot, and Nyberg (2009) used an E-cadherin blocking antibody to inhibit the E-cadherin function on hepatocyte spheroids, which led to an improved cellular death through a caspase-independent mechanism. Liang et al (2016) also demonstrated that the E-cadherin knockdown in HCT116 colorectal cancer cells leads to a decrease on the MDR1 expression in spheroids. The data indicate that E-cadherins can mediate the spheroids drug resistance because of their influence on MDR1 levels via HIF factor-1α (HIF-1α; Liang et al, 2016).…”

Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 85%

“…Liang et al (2016) also demonstrated that the E-cadherin knockdown in HCT116 colorectal cancer cells leads to a decrease on the MDR1 expression in spheroids. The data indicate that E-cadherins can mediate the spheroids drug resistance because of their influence on MDR1 levels via HIF factor-1α (HIF-1α; Liang et al, 2016).…”

Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 85%

“…The results obtained demonstrate that the administration of SHE78-7 improves the intracellular accumulation of the chemotherapeutics (5-FU, etoposide, paclitaxel, and vinblastine) in HT-29 human colorectal cancer spheroids (Green et al, 2004). In a similar approach, Luebke-Wheeler, Nedredal, Yee, Amiot, and Nyberg (2009) Liang et al, 2016). In a similar approach, Luebke-Wheeler, Nedredal, Yee, Amiot, and Nyberg (2009) Liang et al, 2016).…”

Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 96%

“…Because the resistance to chemotherapy and cancer relapse are major clinical challenges attributed to a subpopulation of CSC, several agents that target CSC-associated cell surface receptors (e.g., CD44), signaling pathways (e.g., Notch and Wnt) and ABC efflux transporters are now in clinical trials- Figure 3 Costa, Gaspar, Coutinho, & Correia, 2014;Ivascu & Kubbies, 2007;Tomlinson, Alpaugh, & Barsky, 2001), hepatocyte (Takei et al, 2005), prostate cancer (Enmon, O'Connor, Song, Lacks, & Schwartz, 2002), and renal carcinoma spheroids (Shimazui et al, 2004). Moreover, several studies already revealed that the expression of E-cadherins is more evident in spheroids than in 2D cultures Liang, Xu, Wang, Li, & He, 2016;Xu et al, 2014). For instance, E-cadherins expression was more than fivefolds higher in 14 days old spheroids, formed with carcinoma cells derived from differentiated hepatocytes (Huh7), than in their 2D cell cultures .…”

Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 99%

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3D tumor spheroids as in vitro models to mimic in vivo human solid tumors resistance to therapeutic drugs

Nunes

Barros

Costa

et al. 2018

Biotech & Bioengineering

513

445

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Three-dimensional cell culture models, such as spheroids, can be used in the process of the development of new anticancer agents because they are able to closely mimic the main features of human solid tumors, namely their structural organization, cellular layered assembling, hypoxia, and nutrient gradients. These properties imprint to the spheroids an anticancer therapeutics resistance profile, which is similar to that displayed by human solid tumors. In this review, an overview of the drug resistance mechanisms observed in 3D tumor spheroids is provided. Furthermore, comparisons between the therapeutics resistance profile exhibited by spheroids, and 2D cell cultures are presented. Finally, examples of the therapeutic approaches that have been developed to surpass the drug resistance mechanisms exhibited by spheroids are described. HIGHLIGHTS•The suitability of 3D cell culture models for drug screening purposes is highlighted. •Spheroids and in vivo human solid tumors structural and functional similarities are emphasized.•The drug resistance mechanisms exhibited by spheroids are described.•Therapeutic approaches used to surpass spheroids' drug resistance mechanisms are described. K E Y W O R D Sdrug resistance, drugs, in vitro models, solid tumors, spheroids

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Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 85%

Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 85%

Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 96%

Section: Presence Of Cancer Stem Cells (Csc)mentioning

confidence: 99%

See 2 more Smart Citations

3D tumor spheroids as in vitro models to mimic in vivo human solid tumors resistance to therapeutic drugs

Nunes

Barros

Costa

et al. 2018

Biotech & Bioengineering

513

445

View full text Add to dashboard Cite

show abstract

“…Western blot was performed as previously described 14-15. Cells were lysed in RIPA buffer with protease inhibitors and phosphatase inhibitors for 30 minutes on ice.…”

Section: Methodsmentioning

confidence: 99%

Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation

He¹,

Li²,

Jiang³

et al. 2017

J. Cancer

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Purpose To investigate the correlation between chemoresistance of colorectal cancer to 5-fluorouracil and BNIP3 and the underlying mechanism.Methods BNIP3 protein in specimens was evaluated using immunohistochemistry. Semi-quantitative reverse transcription PCR and Western blot was employed to assay gene expression. The promoter methylation status of BNIP3 was examined by methylation-specific PCR. Drug sensitivity was assayed using MTT assay.Results Specimens from 81 patients with colorectal cancer receiving 5-fluorouracil-based chemotherapy were analyzed. BNIP3 expression was negative in 42 cancer samples. The mean score of BNIP3 in cancer was 1.8±0.2 and it was 3.7±0.5 in adjacent colorectum (p<0.05). The response rate of the BNIP3 positive group was 63.6% and that of the negative group was 36.4% (p=0.021). The median PFS of the BNIP3 positive group was 9.25 months and that of the BNIP3 negative group was 6.5 months (p=0.011). BNIP3 mRNA was not detectable in 4 of 8 colorectal cell lines and all these 4 cell lines displayed BNIP3 methylated allele only. Other 4 cell lines what expressed detectable BNIP3 displayed BNIP3 unmethylated allele only or both unmethylated and methylated alleles. 5-Aza dramatically increased BNIP3 expression. Knockdown of DNMT1 increased BNIP3. Knockdown of DNMT3B alone did not detectably change BNIP3 expression while knockdown of both DNMT1 and DNMT3B increased BNIP3 expression more than knockdown of DNMT1 alone. Knockdown of BNIP3 decreased chemosensitivity to 5-fluorouracil and increasing BNIP3 through demethylation increased chemosensitivity.Conclusion Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation via DNMT1/DNMT3B.

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miR-145 sensitizes gallbladder cancer to cisplatin by regulating multidrug resistance associated protein 1

et al. 2016

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Gallbladder cancer (GBC) is the most common malignancy in biliary tract with poor prognosis. Due to its high chemoresistance, systemic chemotherapies have had limited success in treating GBC patients. MicroRNAs (miRNAs) are emerging novel regulators of chemoresistance, which modulate the expression of drug resistance-related genes. In this study, we investigated the association between miR-145 expression and cisplatin sensitivity by both in vivo and in vitro analysis. Quantitative PCR (q-PCR) analysis indicated an increased miR-145 expression in GBC tissues. In addition, studies on GBC cell lines suggested an increased cisplatin efficacy with miR-145 overexpression, whereas decreasing miR-145 expression reduced cisplatin sensitivity. Further, we found that miR-145 accelerated MRP1 mRNA degradation by directly targeting its 3'-UTR and therefore caused increased cisplatin toxicity in GBC cells. Moreover, lower miR-145 and higher MRP1 expression levels predicted poor prognosis in GBC patients who received chemotherapy. Collectively, our findings established a rationale for using miR-145 expression as a biomarker to identify cisplatin-resistant GBC patients and propose that treatment strategies increasing the expression of miR-145 could be a new therapeutic approach for GBC patients.

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E-cadherin increasing multidrug resistance protein 1 via hypoxia-inducible factor-1α contributes to multicellular resistance in colorectal cancer

Cited by 18 publications

References 34 publications

3D tumor spheroids as in vitro models to mimic in vivo human solid tumors resistance to therapeutic drugs

3D tumor spheroids as in vitro models to mimic in vivo human solid tumors resistance to therapeutic drugs

Chemoresistance of colorectal cancer to 5-fluorouracil is associated with silencing of the BNIP3 gene through aberrant methylation

miR-145 sensitizes gallbladder cancer to cisplatin by regulating multidrug resistance associated protein 1

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