Anion-exchange membranes (AEM) with high ion content usually suffer from excessive water absorption and dilution effects that impair conductivity and mechanical properties. We herein report a novel ether containing a cross-linking strategy without adopting high ion-exchange capacity (IEC). The ether-containing cross-links and the quaternized structure are created simultaneously by introducing an ether-containing flexible hydrophilic spacer between two 1,4-diazabicyclo­[2,2,2,2]­octane or DABCO molecules; the resultant bi-DABCO structure was further employed to react with chloromethylated polysulfone. The long spacer with the ether moiety may benefit the hydroxide ion transport, and the cross-links will control the swelling and water absorption of the AEM. The two ether groups in the long spacer of the cross-links will also shield the DABCO cation from OH– attack due to an electron-donating effect. The prepared membranes exhibited an improved conductivity of 31 mS/cm (at 25 °C) at a comparatively low IEC (1.08 mmol/g) with a rational water absorption and low swelling ratio (95.0 and 27.1%, respectively); they also displayed an enhanced alkaline stability in 1 M NaOH aqueous solution at 80 °C for 150 h. The density functional theory study and physical characterization after the alkaline treatment further confirm the better chemical stability of the cross-linked membrane over its counterpart. Our work presents an effective strategy to balance AEM conductivity and robustness.

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The oncogenic phosphatase PRL-3 is highly expressed in metastatic colorectal cancer but not in nonmetastatic colorectal cancer or noncolorectal cancer metastatic cancers. Although the proinvasive capacity of PRL-3 has been validated in multiple types of cancer, its impact on colorectal cancer progression and the underlying mechanisms remain poorly understood. Here, we report that overexpressed PRL-3 stimulates G 2 -M arrest, chromosomal instability (CIN), self-renewal, and growth of colorectal cancer cells in xenograft models, while colorectal cancer cell proliferation is decreased. PRL-3induced G 2 -M arrest was associated with decreased expression of Aurora kinase A (AURKA). PRL-3-promoted slow proliferation, CIN, self-renewal, and growth in xenografts were counteracted by ectopic expression of AURKA. Conversely, knockdown of PRL-3 resulted in low proliferation, S-phase arrest, impaired self-renewal, increased apoptosis, and diminished xenograft growth independently of AURKA. Analysis of colo-rectal cancer specimens showed that expression of PRL-3 was associated with high status of CIN and poor prognosis, which were antagonized by expression of AURKA. PRL-3 enhanced AURKA ubiquitination and degradation in a phosphatasedependent fashion. PRL-3 interacted with AURKA and FZR1, a regulatory component of the APC/C FZR1 complex. Destabilization of AURKA by PRL-3 required PRL-3-mediated dephosphorylation of FZR1 and assembly of the APC/C FZR1 complex. Our study suggests that PRL-3-regulated colorectal cancer progression is collectively determined by distinct malignant phenotypes and further reveals PRL-3 as an essential regulator of APC/C FZR1 in controlling the stability of AURKA.Significance: Dephosphorylation of FZR1 by PRL-3 facilitates the activity of APC/C FZR1 by destabilizing AURKA, thus influencing aggressive characteristics and overall progression of colorectal cancer.