Dataset Information

Dynamics of gene expression changes in epithelial and mesenchymal HMLER cell lines transitioning from suspension 3D culture to adhesion cultures

ABSTRACT: In order to metastasize, few cells need to detach from the primary tumor, and transition through the circulation to distant sites to establish new solid tumor metastases. The gene expression changes occurring between these transitions are poorly understood, and controversial findings have been reported regarding transitions between epithelial (E) and mesenchymal (M) cell states. To model the metastasis process in vitro, here we examined the dynamics of gene expression changes and respective cell fates that are occurring in cells that are transitioning from adhesion culture to suspension 3D culture (mammospheres) and back to adhesion culture in vitro. We found that mammosphere and replating cultures of epithelial (E) cell lines (HP cells and E clones) led to enrichment for mesenchymal (M) signatures characteristic of the mesenchymal cell lines, indicative of an epithelial to mesenchymal transition (EMT), but retainment of E-specific signatures (Grosse-Wilde et al., 2015). This co-expression of E and M signatures was stably maintained between the mammosphere state in suspension and in replated cells, indicating a stable E/M gene expression state by partial EMT in E cell lines, which has been associated with a stem-like state (Grosse-Wilde et al., 2015; Jolly et al., 2014; Lu et al., 2014; Zhang et al., 2014). Interestingly, mammosphere suspension culture of mesenchymal M clones also resulted in co-expression of E and M signatures generated by partial mesenchymal to epithelial transition (MET). However, in stark contrast to E clones and HP cells, immediately upon replating M cell-derived mammospheres to adhesion lost the intermediate E/M state and converted back to stable expression of M signatures indicative of rapid EMT. This suggests that the intermediate state in M cells is very unstable. Together, these replating data suggest that prolonged detachment of epithelial-derived cells leads to loss of expression of E signatures and EMT. Life-threatening macrometastases typically recapitulate the gene expression of the primary tumor, which requires expression of E signatures, while the mesenchymal micrometastases are frequent but not-proliferative and harmless. Since all HMLER cell lines independent of their initial E or M state converged to an M state upon expansion in suspension, our data suggest that induction of EMT in suspended HMLER cells may be one reason for the observed benign non-metastatic character of HMLER cells when used in mouse xenograft experiments, and for their metastatic inefficiency. Our datasets of the replating kinetic may be useful to identify which pathways are involved in the processes enabling the mixed HP population to maintain a stable E/M expression signature and a more stem-like state, which we have identified as caused by cell-cell cooperation between phenotypically different E and M cell-types. By contrast, M cells can only transiently assume this E/M gene expression state, and not generate a stable phenotypic heterogeneity and therefore absence of cooperation between E and M cell-types. Instability of the intermediate stem-like E/M state in M cell-types and rapid conversion to the M state can explain why 1) pure M populations are often phenotypically stable and are not undergoing MET in vitro (Schmidt et al., 2015; Zhang et al., 2014), 2) why pure M populations are less aggressive resulting in less metastases than mixed cooperating E and M cell populations (Ocaña et al., 2012; Tsuji et al., 2008) or 3) why complete EMT results in more benign less metastasizing tumors than incomplete EMT (Tran et al., 2014; Tsai et al., 2012) and finally 4) why expression of M traits in primary tumors are associated with good patient outcomes and less metastases than E signatures (Kim et al., 2011; Mylona et al., 2008; Tan et al., 2014). Dontu, G., Abdallah, W.M., Foley, J.M., Jackson, K.W., Clarke, M.F., Kawamura, M.J., and Wicha, M.S. (2003). In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells. Genes Dev. 17, 1253–1270. Elenbaas, B., Spirio, L., Koerner, F., Fleming, M.D., Zimonjic, D.B., Donaher, J.L., Popescu, N.C., Hahn, W.C., and Weinberg, R.A. (2001). Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells. Genes Dev 15, 50–65. Grosse-Wilde, A., Fouquier d’Hérouël, A., McIntosh, E., Ertaylan, G., Skupin, A., Kuestner, R.E., del Sol, A., Walters, K.-A., and Huang, S. (2015). Stemness of the hybrid Epithelial/Mesenchymal State in Breast Cancer and Its Association with Poor Survival. PLOS ONE 10, e0126522. Jolly, M.K., Huang, B., Lu, M., Mani, S.A., Levine, H., and Ben-Jacob, E. (2014). Towards elucidating the connection between epithelial-mesenchymal transitions and stemness. J. R. Soc. Interface R. Soc. 11, 20140962. Kim, H.J., Kim, M.-J., Ahn, S.H., Son, B.H., Kim, S.B., Ahn, J.H., Noh, W.C., and Gong, G. (2011). Different prognostic significance of CD24 and CD44 expression in breast cancer according to hormone receptor status. The Breast 20, 78–85. Lu, M., Jolly, M.K., Onuchic, J., and Ben-Jacob, E. (2014). Toward decoding the principles of cancer metastasis circuits. Cancer Res. 74, 4574–4587. Mylona, E., Giannopoulou, I., Fasomytakis, E., Nomikos, A., Magkou, C., Bakarakos, P., and Nakopoulou, L. (2008). The clinicopathologic and prognostic significance of CD44+/CD24−/low and CD44−/CD24+ tumor cells in invasive breast carcinomas. Hum. Pathol. 39, 1096–1102. Ocaña, O.H., Córcoles, R., Fabra, Á., Moreno-Bueno, G., Acloque, H., Vega, S., Barrallo-Gimeno, A., Cano, A., and Nieto, M.A. (2012). Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1. Cancer Cell 22, 709–724. Schmidt, J.M., Panzilius, E., Bartsch, H.S., Irmler, M., Beckers, J., Kari, V., Linnemann, J.R., Dragoi, D., Hirschi, B., Kloos, U.J., et al. (2015). Stem-Cell-like Properties and Epithelial Plasticity Arise as Stable Traits after Transient Twist1 Activation. Cell Rep. 10, 131–139. Tan, T.Z., Miow, Q.H., Miki, Y., Noda, T., Mori, S., Huang, R.Y.-J., and Thiery, J.P. (2014). Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients. EMBO Mol. Med. 6, 1279–1293. Tran, H.D., Luitel, K., Kim, M., Zhang, K., Longmore, G.D., and Tran, D.D. (2014). Transient SNAIL1 Expression Is Necessary for Metastatic Competence in Breast Cancer. Cancer Res. 74, 6330–6340. Tsai, J.H., Donaher, J.L., Murphy, D.A., Chau, S., and Yang, J. (2012). Spatiotemporal Regulation of Epithelial-Mesenchymal Transition Is Essential for Squamous Cell Carcinoma Metastasis. Cancer Cell 22, 725–736. Tsuji, T., Ibaragi, S., Shima, K., Hu, M.G., Katsurano, M., Sasaki, A., and Hu, G. -f. (2008). Epithelial-Mesenchymal Transition Induced by Growth Suppressor p12CDK2-AP1 Promotes Tumor Cell Local Invasion but Suppresses Distant Colony Growth. Cancer Res. 68, 10377–10386. Zhang, J., Tian, X.-J., Zhang, H., Teng, Y., Li, R., Bai, F., Elankumaran, S., and Xing, J. (2014). TGF- -induced epithelial-to-mesenchymal transition proceeds through stepwise activation of multiple feedback loops. Sci. Signal. 7, ra91–ra91.

ORGANISM(S): Homo sapiens

PROVIDER: GSE70279 | GEO | 2015/07/10

SECONDARY ACCESSION(S): PRJNA288149

REPOSITORIES: GEO

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Project description:In order to metastasize, few cells need to detach from the primary tumor, and transition through the circulation to distant sites to establish new solid tumor metastases. The gene expression changes occurring between these transitions are poorly understood, and controversial findings have been reported regarding transitions between epithelial (E) and mesenchymal (M) cell states. To model the metastasis process in vitro, here we examined the dynamics of gene expression changes and respective cell fates that are occurring in cells that are transitioning from adhesion culture to suspension 3D culture (mammospheres) and back to adhesion culture in vitro. We found that mammosphere and replating cultures of epithelial (E) cell lines (HP cells and E clones) led to enrichment for mesenchymal (M) signatures characteristic of the mesenchymal cell lines, indicative of an epithelial to mesenchymal transition (EMT), but retainment of E-specific signatures (Grosse-Wilde et al., 2015). This co-expression of E and M signatures was stably maintained between the mammosphere state in suspension and in replated cells, indicating a stable E/M gene expression state by partial EMT in E cell lines, which has been associated with a stem-like state (Grosse-Wilde et al., 2015; Jolly et al., 2014; Lu et al., 2014; Zhang et al., 2014). Interestingly, mammosphere suspension culture of mesenchymal M clones also resulted in co-expression of E and M signatures generated by partial mesenchymal to epithelial transition (MET). However, in stark contrast to E clones and HP cells, immediately upon replating M cell-derived mammospheres to adhesion lost the intermediate E/M state and converted back to stable expression of M signatures indicative of rapid EMT. This suggests that the intermediate state in M cells is very unstable. Together, these replating data suggest that prolonged detachment of epithelial-derived cells leads to loss of expression of E signatures and EMT. Life-threatening macrometastases typically recapitulate the gene expression of the primary tumor, which requires expression of E signatures, while the mesenchymal micrometastases are frequent but not-proliferative and harmless. Since all HMLER cell lines independent of their initial E or M state converged to an M state upon expansion in suspension, our data suggest that induction of EMT in suspended HMLER cells may be one reason for the observed benign non-metastatic character of HMLER cells when used in mouse xenograft experiments, and for their metastatic inefficiency. Our datasets of the replating kinetic may be useful to identify which pathways are involved in the processes enabling the mixed HP population to maintain a stable E/M expression signature and a more stem-like state, which we have identified as caused by cell-cell cooperation between phenotypically different E and M cell-types. By contrast, M cells can only transiently assume this E/M gene expression state, and not generate a stable phenotypic heterogeneity and therefore absence of cooperation between E and M cell-types. Instability of the intermediate stem-like E/M state in M cell-types and rapid conversion to the M state can explain why 1) pure M populations are often phenotypically stable and are not undergoing MET in vitro (Schmidt et al., 2015; Zhang et al., 2014), 2) why pure M populations are less aggressive resulting in less metastases than mixed cooperating E and M cell populations (Ocaña et al., 2012; Tsuji et al., 2008) or 3) why complete EMT results in more benign less metastasizing tumors than incomplete EMT (Tran et al., 2014; Tsai et al., 2012) and finally 4) why expression of M traits in primary tumors are associated with good patient outcomes and less metastases than E signatures (Kim et al., 2011; Mylona et al., 2008; Tan et al., 2014). Dontu, G., Abdallah, W.M., Foley, J.M., Jackson, K.W., Clarke, M.F., Kawamura, M.J., and Wicha, M.S. (2003). In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells. Genes Dev. 17, 1253–1270. Elenbaas, B., Spirio, L., Koerner, F., Fleming, M.D., Zimonjic, D.B., Donaher, J.L., Popescu, N.C., Hahn, W.C., and Weinberg, R.A. (2001). Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells. Genes Dev 15, 50–65. Grosse-Wilde, A., Fouquier d’Hérouël, A., McIntosh, E., Ertaylan, G., Skupin, A., Kuestner, R.E., del Sol, A., Walters, K.-A., and Huang, S. (2015). Stemness of the hybrid Epithelial/Mesenchymal State in Breast Cancer and Its Association with Poor Survival. PLOS ONE 10, e0126522. Jolly, M.K., Huang, B., Lu, M., Mani, S.A., Levine, H., and Ben-Jacob, E. (2014). Towards elucidating the connection between epithelial-mesenchymal transitions and stemness. J. R. Soc. Interface R. Soc. 11, 20140962. Kim, H.J., Kim, M.-J., Ahn, S.H., Son, B.H., Kim, S.B., Ahn, J.H., Noh, W.C., and Gong, G. (2011). Different prognostic significance of CD24 and CD44 expression in breast cancer according to hormone receptor status. The Breast 20, 78–85. Lu, M., Jolly, M.K., Onuchic, J., and Ben-Jacob, E. (2014). Toward decoding the principles of cancer metastasis circuits. Cancer Res. 74, 4574–4587. Mylona, E., Giannopoulou, I., Fasomytakis, E., Nomikos, A., Magkou, C., Bakarakos, P., and Nakopoulou, L. (2008). The clinicopathologic and prognostic significance of CD44+/CD24−/low and CD44−/CD24+ tumor cells in invasive breast carcinomas. Hum. Pathol. 39, 1096–1102. Ocaña, O.H., Córcoles, R., Fabra, Á., Moreno-Bueno, G., Acloque, H., Vega, S., Barrallo-Gimeno, A., Cano, A., and Nieto, M.A. (2012). Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1. Cancer Cell 22, 709–724. Schmidt, J.M., Panzilius, E., Bartsch, H.S., Irmler, M., Beckers, J., Kari, V., Linnemann, J.R., Dragoi, D., Hirschi, B., Kloos, U.J., et al. (2015). Stem-Cell-like Properties and Epithelial Plasticity Arise as Stable Traits after Transient Twist1 Activation. Cell Rep. 10, 131–139. Tan, T.Z., Miow, Q.H., Miki, Y., Noda, T., Mori, S., Huang, R.Y.-J., and Thiery, J.P. (2014). Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients. EMBO Mol. Med. 6, 1279–1293. Tran, H.D., Luitel, K., Kim, M., Zhang, K., Longmore, G.D., and Tran, D.D. (2014). Transient SNAIL1 Expression Is Necessary for Metastatic Competence in Breast Cancer. Cancer Res. 74, 6330–6340. Tsai, J.H., Donaher, J.L., Murphy, D.A., Chau, S., and Yang, J. (2012). Spatiotemporal Regulation of Epithelial-Mesenchymal Transition Is Essential for Squamous Cell Carcinoma Metastasis. Cancer Cell 22, 725–736. Tsuji, T., Ibaragi, S., Shima, K., Hu, M.G., Katsurano, M., Sasaki, A., and Hu, G. -f. (2008). Epithelial-Mesenchymal Transition Induced by Growth Suppressor p12CDK2-AP1 Promotes Tumor Cell Local Invasion but Suppresses Distant Colony Growth. Cancer Res. 68, 10377–10386. Zhang, J., Tian, X.-J., Zhang, H., Teng, Y., Li, R., Bai, F., Elankumaran, S., and Xing, J. (2014). TGF- -induced epithelial-to-mesenchymal transition proceeds through stepwise activation of multiple feedback loops. Sci. Signal. 7, ra91–ra91. For these analyses we used the heterogeneous parental HMLER (HP) cell line, with isogenic epithelial (E) and mesenchymal (M) cell-types (Elenbaas et al., 2001), and stable clonal HMLER-derived E and M cell lines, which are normally passaged under adhesion conditions (_adh, GSE66527). We cultured cell lines under 3D suspension conditions resembling mammosphere growth conditions that are typically used to enrich for stem-like cells (Dontu et al., 2003), and examined gene expression of cells under mammosphere conditions (_sus, GSE66527), or after replating (_re) in a kinetic examining gene expression from 6, 24, 96, and 240 hrs after cells were allowed to readhere to normal dishes for the heterogeneous but mostly epithelial (HP) cell lines and mesenchymal (M4) cell lines. To validate our findings we also examined gene expression of cells replated after mammosphere culture for about two weeks from three different E (E3, E4, E5) and M clones (M3, M4, M1). All gene expression samples were taken from biological replicates (at least duplicates) of cells grown in different wells or even at different times. Gene expression of replated (_re) cells was compared to the respective cell lines grown under adhesion conditions (_adh), as well as to the respective cell line grown under suspension mammosphere condition (_sus) which have been deposited previously under accession number GSE66527. HP replicates (re): HP_re_AGW120913, HP_re_RK12026, HP_re_AGW1209_5, HP_re_AGW1209_6, HP_re_AGW1209_7, HP_re_AGW1209_8, HP_re_AGW1209_9, HP_re_0607_1, HP_re_0607_2 E3 replicates (re): E3_re_RK1202, E3_re_RK12028; E4 replicates: E4_re_0622, E4_re_0613; E5 replicates: E5_re_0613_1, E5_re_0613_2 M1 replicates (re): M1_re_0607_1, M1_re_0607_2, M2 replicates: M2_re_RK1202, M2_re_RK12029, M2_re_AGW1209_3, M2_re_AGW1209_4, M2_re_AGW1209_5, M3 replicates: M4_re_0607_1, M4_re_0607_2 HP replicates (adh): HP_adh_0629, HP_adh_2210, HP_adh_0607sc, HP_adh_0607c E3 replicates (adh): E3_adh_0629, E3_adh, E3_adh_0826. E4 replicates (adh): E4_adh_0607, E4_adh_0210, E5 replicates (adh): E5_adh_0210, E5_adh_0607 M1 replicates (adh): M1_adh_0210, M1_adh_0607, M4 replicates (adh): M4_adh_0607, M4_adh_0210, M3 replicates (adh): M3_adh, M3_adh_2210, M3_adh_2810 HP replating kinetic (adh): HP_adh_0607c (GSE66527), HP_adh_0607sc (GSE66527), HP (mammospheres, suspension): HP_sus_0603_2 (GSE66527), HP_sus_0603_1 (GSE66527), HP (replated 6 hrs): HP_re_6_0603_1, HP_re_6_0603_2, HP (replated 24hrs): HP_re_24_0607_1, HP_re_24_0607_2, HP (replated 96 hrs): HP_re_96_0607_1, HP_re_96_0607_2, HP (replated 240hrs): HP_re_0607_1, HP_re_0607_2, M4 replating kinetic (adh): M4_adh_0210 (GSE66527), M4_adh_0607 (GSE66527), M4 (mammospheres, suspension): M4_sus_0603_2 (GSE66527), M4_sus_0603_1 (GSE66527), M4 (replated 24 hrs): M4_re_24_0603_1, M4_re_24_0603_2, M4 (replated 96 hrs), M4_re_96_0607_1, M4_re_96_0607_2, M4 replated 240hrs): M4_re_0607_1, M4_re_0607_2

Project description:CD47 is a transmembrane glycoprotein that is ubiquitously expressed in different organs and tissues (Barclay and Van den Berg 2014; Liu, et al. 2017). In the human immune system, CD47 interacts with some integrins, two counter-receptor signal regulator protein (SIRP) family members, and the secreted thrombospondin-1 (TSP1) (Barclay and Van den Berg 2014; Gao, et al. 2016; Kaur, et al. 2013; Oldenborg, et al. 2000). CD47 has two established roles in the immune system. The CD47-SIRPα interaction was identified as a critical innate immune checkpoint, which delivers an antiphagocytic signal to macrophages and inhibits neutrophil cytotoxicity (Martínez- Sanz, et al. 2021). Its interaction with inhibitory SIRPα is a physiological anti-phagocytic “don’t eat me” signal on circulating red blood cells that is co-opted by cancer cells (Matlung, et al. 2017). Many malignant cells overexpress CD47 (Betancur, et al. 2017; Chao, et al. 2011; Jaiswal, et al. 2009; Majeti, et al. 2009; Oronsky, et al. 2020; Petrova, et al. 2017). CD47/SIRPα-targeted therapeutics have been developed to overcome this immune checkpoint for cancer treatment (Kaur, et al. 2020; Matlung, et al. 2017). Secondly, engagement of CD47 on T cells by TSP1 regulates their differentiation and survival (Grimbert, et al. 2006; Lamy, et al. 2007) and inhibits T cell receptor signaling and antigen presentation by dendritic cells (DCs) (Kaur, et al. 2014; Li, et al. 2002; Liu, et al. 2015; Miller, et al. 2013; Soto-Pantoja, et al. 2014; Weng, et al. 2014). TSP1/CD47 signaling has similar inhibitory functions to limit NK cell activation (Kim, et al. 2008; Nath, et al. 2018; Nath, et al. 2019; Schwartz, et al. 2019) and IL1β production by macrophages (Stein, et al. 2016). CD47 is therefore a checkpoint that regulates both innate and adaptive immunity. The recent understanding of CD47 antagonism associated with increased antigen presentation by DCs (Liu, et al. 2016) and natural killer cell cytotoxicity (Nath, et al. 2019) contributes to the heightened interest in CD47 as a therapeutic target (Kaur, et al. 2020).

Project description:Our group is interested in epithelial-to-mesenchymal transition (EMT), in particular, TGF-beta induced EMT. TGF-beta signalling has been shown to be an important factor in the induction of EMT and it has been demonstrated that adding TGF-beta to epithelial cells in culture is a convenient way to study the process of EMT. In response to TGF-beta, Smad2 and 3 are activated, and form complexes with Smad4, which then regulate transcription of target genes through interactions with other DNA binding transcription factors. In the induction of EMT, the activated Smads mediate transcriptional regulation through three families of transcription factors, resulting in repression of epithelial marker gene expression and activation of mesenchymal gene expression (Xu J, et al. 2009) Also investigated in this study is the role of H2A.Z in EMT. H2A.Z is an evolutionary conserved and a metazoan essential histone variant of the H2A class. Mice deficient in H2A.Z die during early development but the reason for this is unknown (Faast et al. 2001). Previously, our laboratory showed that the loss of H2A.Z in Xenpous laevis impaired cell movement required for the formation of the mesoderm and neural crest (Ridgway et al. 2004). Given that mesoderm formation is critically dependent upon EMT, we therefore wondered whether H2A.Z might be a chromatin regulator of EMT. We transfected MDCK cells with a lentiviral vector to express a construct encoding an shRNA targeting canine H2A.Z as we wanted to test the hypothesis that H2A.Z is involved in the maintenance of cellular identity and that its loss might trigger de-differentiation. In order to investigate changes in histone variant H2A.Z occupancy associated with TGF-beta induced epithelial-to-mesenchymal transition (EMT) we performed H2A.Z ChIP-Seq in untreated and TGFb-treated MDCK cells. The MDCK cell line has been extensively used as a model system for EMT because they convert fully from the epithelial to the mesenchymal state in response to TGF-beta. Please note that RNA-seq data generated in conjunction to this ChIP-seq data set were also deposited at ArrayExpress under accession number E-MTAB-5628 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5628 ).

Project description:Our group is interested in epithelial-to-mesenchymal transition (EMT), in particular, TGF-beta induced EMT. TGF-beta signalling has been shown to be an important factor in the induction of EMT and it has been demonstrated that adding TGF-beta to epithelial cells in culture is a convenient way to study the process of EMT. âIn response to TGF-beta, Smad2 and 3 are activated, and form complexes with Smad4, which then regulate transcription of target genes through interactions with other DNA binding transcription factors. In the induction of EMT, the activated Smads mediate transcriptional regulation through three families of transcription factors, resulting in repression of epithelial marker gene expression and activation of mesenchymal gene expressionâ (Xu J, et al. 2009) Also investigated in this study is the role of H2A.Z in EMT. H2A.Z is an evolutionary conserved and a metazoan essential histone variant of the H2A class. Mice deficient in H2A.Z die during early development but the reason for this is unknown (Faast et al. 2001). Previously, our laboratory showed that the loss of H2A.Z in Xenpous laevis impaired cell movement required for the formation of the mesoderm and neural crest (Ridgway et al. 2004). Given that mesoderm formation is critically dependent upon EMT, we therefore wondered whether H2A.Z might be a chromatin regulator of EMT. We transfected MDCK cells with a lentiviral vector to express a construct encoding an shRNA targeting canine H2A.Z as we wanted to test the hypothesis that H2A.Z is involved in the maintenance of cellular identity and that its loss might trigger de-differentiation. In order to investigate changes in gene expression associated with TGF-beta induced epithelial-to-mesenchymal transition (EMT) we performed paired end RNA-Seq of poly-A selected mRNA in untreated and TGFb-treated MDCK cells. The MDCK cell line has been extensively used as a model system for EMT because they convert fully from the epithelial to the mesenchymal state in response to TGF-beta. Gene expression profiles were also generated from MDCK cells in which H2A.Z was knocked down using shRNA. Please note that ChIP-seq data generated in conjunction to this RNA-seq data set were also deposited at ArrayExpress under accession number E-MTAB-5637 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5637 ).

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Dynamics of gene expression changes in epithelial and mesenchymal HMLER cell lines transitioning from suspension 3D culture to adhesion cultures

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